Статті в журналах: "GITC"

1

Nocero, M., T. Isshiki, M. Yamamoto, and C. S. Hoffman. "Glucose repression of fbp1 transcription of Schizosaccharomyces pombe is partially regulated by adenylate cyclase activation by a G protein alpha subunit encoded by gpa2 (git8)." Genetics 138, no. 1 (September 1, 1994): 39–45. http://dx.doi.org/10.1093/genetics/138.1.39.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Abstract In the fission yeast Schizosaccharomyces pombe, genetic studies have identified genes that are required for glucose repression of fbp1 transcription. The git2 gene, also known as cyr1, encodes adenylate cyclase. Adenylate cyclase converts ATP into the second messenger cAMP as part of many eukaryotic signal transduction pathways. The git1, git3, git5, git7, git8 and git10 genes act upstream of adenylate cyclase, presumably encoding an adenylate cyclase activation pathway. In mammalian cells, adenylate cyclase enzymatic activity is regulated by heterotrimeric guanine nucleotide-binding proteins (G proteins). In the budding yeast Saccharomyces cerevisiae, adenylate cyclase enzymatic activity is regulated by monomeric, guanine nucleotide-binding Ras proteins. We show here that git8 is identical to the gpa2 gene that encodes a protein homologous to the alpha subunit of a G protein. Mutations in two additional genes, git3 and git5 are suppressed by gpa2+ in high copy number. Furthermore, a mutation in either git3 or git5 has an additive effect in strains deleted for gpa2 (git8), as it significantly increases expression of an fbp1-lacZ reporter gene. Therefore, git3 and git5 appear to act either in concert with or independently from gpa2 (git8) to regulate adenylate cyclase activity.

2

Welton, Robert M., та Charles S. Hoffman. "Glucose Monitoring in Fission Yeast via the gpa2 Gα, the git5 Gβ and the git3 Putative Glucose Receptor". Genetics 156, № 2 (1 жовтня 2000): 513–21. http://dx.doi.org/10.1093/genetics/156.2.513.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Abstract The fission yeast Schizosaccharomyces pombe responds to environmental glucose by activating adenylate cyclase. The resulting cAMP signal activates protein kinase A (PKA). PKA inhibits glucose starvation-induced processes, such as conjugation and meiosis, and the transcription of the fbp1 gene that encodes the gluconeogenic enzyme fructose-1,6-bisphosphatase. We previously identified a collection of git genes required for glucose repression of fbp1 transcription, including pka1/git6, encoding the PKA catalytic subunit, git2/cyr1, encoding adenylate cyclase, and six “upstream” genes required for adenylate cyclase activation. The git8 gene, identical to gpa2, encodes the alpha subunit of a heterotrimeric guanine-nucleotide binding protein (Gα) while git5 encodes a Gβ subunit. Multicopy suppression studies with gpa2+ previously indicated that S. pombe adenylate cyclase activation may resemble that of the mammalian type II enzyme with sequential activation by Gα followed by βγ. We show here that an activated allele of gpa2 (gpa2R176H, carrying a mutation in the coding region for the GTPase domain) fully suppresses mutations in git3 and git5, leading to a refinement in our model. We describe the cloning of git3 and show that it encodes a putative seven-transmembrane G protein-coupled receptor. A git3 deletion confers the same phenotypes as deletions of other components of the PKA pathway, including a germination delay, constitutive fbp1 transcription, and starvation-independent conjugation. Since the git3 deletion is fully suppressed by the gpa2R176H allele with respect to fbp1 transcription, git3 appears to encode a G protein-coupled glucose receptor responsible for adenylate cyclase activation in S. pombe.

3

Hoffman, C. S. "Glucose sensing via the protein kinase A pathway in Schizosaccharomyces pombe." Biochemical Society Transactions 33, no. 1 (February 1, 2005): 257–60. http://dx.doi.org/10.1042/bst0330257.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

The fission yeast Schizosaccharomyces pombe primarily detects glucose via a cAMP-signalling pathway. Components of this pathway include the Git3 G-protein-coupled receptor and a heterotrimeric G-protein, from which the Gpa2 Gα subunit activates adenylate cyclase (Git2/Cyr1). Three additional proteins, Git1, Git7 and Git10 are required to generate a cAMP response even in a strain expressing an activated form of Gpa2, which is capable of bypassing the loss of the GPCR and Gβγ dimer. Therefore, Git1, Git7 and Git10 either act in a G-protein-independent manner or are required to stabilize or assemble a functional signalling complex. Although prior data suggested that the Cgs2 cAMP phosphodiesterase (PDE) does not regulate the cAMP response, we now have evidence that along with adenylate cyclase regulation, PDE activation is important for limiting the response to glucose. Finally, regulation of protein kinase A activation appears to involve both traditional post-translational regulation of the function of the components of the cAMP pathway and glucose-dependent transcriptional regulation of some of these cAMP pathway genes.

4

Gilleland, Rebecca C., and Richard D. Hockett. "Stability of RNA Molecules Stored in GITC." BioTechniques 25, no. 6 (December 1998): 944–48. http://dx.doi.org/10.2144/98256bm03.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

5

Anike, US, I. A. Nwannadi, I. Okpala, and AJ Madu. "The Role of Micro-RNA 466i on Vaso-Occlusive Complications of Sickle Cell Anaemia." Journal of BioMedical Research and Clinical Practice 2, no. 2 (July 6, 2019): 144–49. http://dx.doi.org/10.46912/2i2.2019111.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Vaso-occlusion in sickle cell anaemia (SCA) is mediated via increased expression of adhesion molecules. Micro-RNA 466i up regulates the expression of interleukin-10 and may contribute to the pathogenesis of the complications in SCA. We sought to investigate the relationship between changes in the level of micro-RNA 466i and the frequency of vaso-occlusive complications in SCA patients. Red blood cells were lysed using ammonium chloride. The resulting white blood cell pellets were lysed in guanidiumisothiocyanate (GITC) lyses buffer. From the GITC lysate, total RNA was extracted. Thereafter, the amount of micro-RNA 466i was quantified. There were no relationships between microRNA 466i and the frequency of complications in SCA patients. (p=0.066) There was also no significant difference in the levels of micro-RNA 466i between patients who had vaso-occlusive complications and those that did not.(p=0.9307) Micro-RNA 466i increased with age (p=0.03) but there was no significant difference between the males and the females patients.(p= 0.370) Micro-RNA 466i (a pro-inflammatory nucleotide) play little or no role in the pathogenesis of vaso-occlusive complications in SCA. Its assay in this group of patients may is not useful in the overall management of these patients.

6

Anike, US, I. A. Nwannadi, I. Okpala, and AJ Madu. "The Role of Micro-RNA 466i on Vaso-Occlusive Complications of Sickle Cell Anaemia." Journal of BioMedical Research and Clinical Practice 2, no. 2 (July 6, 2019): 144–49. http://dx.doi.org/10.46912/jbrcp.111.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Vaso-occlusion in sickle cell anaemia (SCA) is mediated via increased expression of adhesion molecules. Micro-RNA 466i up regulates the expression of interleukin-10 and may contribute to the pathogenesis of the complications in SCA. We sought to investigate the relationship between changes in the level of micro-RNA 466i and the frequency of vaso-occlusive complications in SCA patients. Red blood cells were lysed using ammonium chloride. The resulting white blood cell pellets were lysed in guanidiumisothiocyanate (GITC) lyses buffer. From the GITC lysate, total RNA was extracted. Thereafter, the amount of micro-RNA 466i was quantified. There were no relationships between microRNA 466i and the frequency of complications in SCA patients. (p=0.066) There was also no significant difference in the levels of micro-RNA 466i between patients who had vaso-occlusive complications and those that did not.(p=0.9307) Micro-RNA 466i increased with age (p=0.03) but there was no significant difference between the males and the females patients.(p= 0.370) Micro-RNA 466i (a pro-inflammatory nucleotide) play little or no role in the pathogenesis of vaso-occlusive complications in SCA. Its assay in this group of patients may is not useful in the overall management of these patients.

7

Anike, US, I. A. Nwannadi, I. Okpala, and AJ Madu. "The Role of Micro-RNA 466i on Vaso-Occlusive Complications of Sickle Cell Anaemia." Journal of BioMedical Research and Clinical Practice 2, no. 2 (July 6, 2019): 144–49. http://dx.doi.org/10.46912/jbrcp.v2.i2.2019.111.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Vaso-occlusion in sickle cell anaemia (SCA) is mediated via increased expression of adhesion molecules. Micro-RNA 466i up regulates the expression of interleukin-10 and may contribute to the pathogenesis of the complications in SCA. We sought to investigate the relationship between changes in the level of micro-RNA 466i and the frequency of vaso-occlusive complications in SCA patients. Red blood cells were lysed using ammonium chloride. The resulting white blood cell pellets were lysed in guanidiumisothiocyanate (GITC) lyses buffer. From the GITC lysate, total RNA was extracted. Thereafter, the amount of micro-RNA 466i was quantified. There were no relationships between microRNA 466i and the frequency of complications in SCA patients. (p=0.066) There was also no significant difference in the levels of micro-RNA 466i between patients who had vaso-occlusive complications and those that did not.(p=0.9307) Micro-RNA 466i increased with age (p=0.03) but there was no significant difference between the males and the females patients.(p= 0.370) Micro-RNA 466i (a pro-inflammatory nucleotide) play little or no role in the pathogenesis of vaso-occlusive complications in SCA. Its assay in this group of patients may is not useful in the overall management of these patients.

8

Schadick, Kevin, H. Matthew Fourcade, Peter Boumenot, Jeffrey J. Seitz, Jennifer L. Morrell, Louise Chang, Kathleen L. Gould, et al. "Schizosaccharomyces pombe Git7p, a Member of the Saccharomyces cerevisiae Sgt1p Family, Is Required for Glucose and Cyclic AMP Signaling, Cell Wall Integrity, and Septation." Eukaryotic Cell 1, no. 4 (August 2002): 558–67. http://dx.doi.org/10.1128/ec.1.4.558-567.2002.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

ABSTRACT The Schizosaccharomyces pombe fbp1 gene, encoding fructose-1,6-bisphosphatase, is transcriptionally repressed by glucose. Mutations that confer constitutive fbp1 transcription identify git (glucose-insensitive transcription) genes that encode components of a cyclic AMP (cAMP) signaling pathway required for adenylate cyclase activation. Four of these genes encode the three subunits of a heterotrimeric G protein (gpa2, git5, and git11) and a G protein-coupled receptor (git3). Three additional genes, git1, git7, and git10, act in parallel to or downstream from the G protein genes. Here, we describe the cloning and characterization of the git7 gene. The Git7p protein is a member of the Saccharomyces cerevisiae Sgt1p protein family. In budding yeast, Sgt1p associates with Skp1p and plays an essential role in kinetochore assembly, while in Arabidopsis, a pair of SGT1 proteins have been found to be involved in plant disease resistance through an interaction with RAR1. Like S. cerevisiae Sgt1p, Git7p is essential, but this requirement appears to be due to roles in septation and cell wall integrity, which are unrelated to cAMP signaling, as S. pombe cells lacking either adenylate cyclase or protein kinase A are viable. In addition, git7 mutants are sensitive to the microtubule-destabilizing drug benomyl, although they do not display a chromosome stability defect. Two alleles of git7 that are functional for cell growth and septation but defective for glucose-triggered cAMP signaling encode proteins that are altered in the highly conserved carboxy terminus. The S. cerevisiae and human SGT1 genes both suppress git7-93 but not git7-235 for glucose repression of fbp1 transcription and benomyl sensitivity. This allele-specific suppression indicates that the Git7p/Sgt1p proteins may act as multimers, such that Git7-93p but not Git7-235p can deliver the orthologous proteins to species-specific targets. Our studies suggest that members of the Git7p/Sgt1p protein family may play a conserved role in the regulation of adenylate cyclase activation in S. pombe, S. cerevisiae, and humans.

9

Schmalzigaug, Robert, Hyewon Phee, Collin E. Davidson, Arthur Weiss, and Richard T. Premont. "Differential Expression of the ARF GAP Genes GIT1 and GIT2 in Mouse Tissues." Journal of Histochemistry & Cytochemistry 55, no. 10 (October 2007): 1039–48. http://dx.doi.org/10.1369/jhc.7a7207.2007.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

GIT1 and GIT2 belong to the family of ADP-ribosylation factor GTPase-activating proteins (ARF-GAP) and have been implicated in the regulation of G protein-coupled receptor sequestration, cell migration, T-cell activation, neuronal spine formation, and aggregate formation in Huntington's disease. Examination of endogenous GIT protein expression in tissues, however, has been hampered by the lack of GIT2-specific antibodies. To visualize GIT1 and GIT2 gene expression in mouse tissues, we created mice with β-galactosidase (β-Gal) reporters inserted into the two GIT genes. β-Gal staining confirmed the broad tissue distribution of GIT1 and GIT2 in the mouse but also revealed striking differences. GIT2 is expressed in most cells of the body, whereas GIT1 is restricted to only a subset of cells. For example, GIT2 is uniformly expressed throughout lung and liver, whereas GIT1 is restricted to cells lining blood vessels, bronchi, and bile ducts. Expression of GIT1 and GIT2 is mutually exclusive in the testes, where a developmental expression shift occurs, with GIT2 present in spermatogonia but GIT1 in mature spermatids. In conclusion, analysis of endogenous GIT expression revealed a nearly ubiquitous distribution of GIT2, whereas GIT1 is restricted to specific cell types even in tissues with apparently high GIT1 expression and is entirely absent from some tissues. (J Histochem Cytochem 55: 1039–1048, 2007)

10

Hartono, Indra K., Novan Zulkarnain, and Rudy Tjahyadi. "Prototype of Dashboard Business Intelligent for Employees Training Effectiveness." Advanced Science Letters 21, no. 4 (April 1, 2015): 661–66. http://dx.doi.org/10.1166/asl.2015.5931.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Employees training in a company is considered as expenditure rather than as a long-term investment by company. The company needs to monitor the training of employees in order to take advantage of the training results by using Business Intelligent (BI). The object of research conducted at Garuda Indonesia Training Center (GITC). Methods of the research is a quantitative, analyze correlation and regression and the variables need to be examine in this research, are as follows: Nature of Training, Management Involvement, Management Motivation, Training Outcome and Firm Performance. Based on this research findings, the hypothesis can be accepted or rejected and hence, a better of prototype of Dashboard Business Intelligent can be well designed and make Employees Training more effective.

11

Pillon, Delphine, and Gilles Bruneau. "Resistant Ribonuclease Activity in Preparations of Total RNA Extracted from Artiodactyl Brain with GITC." BioTechniques 34, no. 5 (May 2003): 920–24. http://dx.doi.org/10.2144/03345bm04.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

12

Nishi, H., N. Fujimura, H. Yamaguchi, W. Jyomori, and T. Fukuyama. "Reversed-phase HPLC separation of the enantiomers of denopamine after derivatization with GITC chiral reagent." Chromatographia 30, no. 3-4 (August 1990): 186–90. http://dx.doi.org/10.1007/bf02274544.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

13

Phee, Hyewon, and Arthur Weiss. "Generation and characterization of GIT1 and GIT2 deficient mice (87.18)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S131. http://dx.doi.org/10.4049/jimmunol.178.supp.87.18.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Abstract The G-protein-coupled receptor (GPCR)-kinase-interacting proteins 1 and 2 (GIT1 and GIT2) are multidomain proteins involved in diverse cellular processes. In fibroblasts, GITs are thought to regulate focal adhesion (FA) turnover, cell spreading, and motility through interaction with various proteins, including Pak-interacting Rac/Cdc42 guanine exchange factor, PIX. In T lymphocytes, GITs interact with alpha and beta PIX and PAK (p21-activated kinase) through their interaction with PIX. Previously, we showed that the GIT/PIX/PAK complex is recruited to the contact site between T cell and antigen presenting cell and GIT and/or PIX seems to play a crucial role in PAK recruitment and T cell activation. However, the physiological roles and activation mechanism of GITs in TCR-activated signal transduction pathways and T cell immune responses have not been addressed thoroughly. GIT1 and GIT2 both are expressed in human and mouse T cells, although the major form expressed in hematopoietic lineage is GIT2. To determine the role of GIT1 and GIT2 in immune cell activation in vivo, we generated GIT1 and GIT2 deficient mice. Both deficient mouse lines were backcrossed to C57BL/6 and Balb/C backgrounds in order to perform functional immunological studies. In the meantime, we performed biochemical studies that do not require pure background.

14

Phee, Hyewon, Marianne N. Mollenauer, and Arthur Weiss. "Role of GIT2 in T cell migration and development (95.8)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 95.8. http://dx.doi.org/10.4049/jimmunol.182.supp.95.8.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Abstract The G-protein-coupled receptor (GPCR)-kinase-interacting proteins (GIT) 1 and 2 are multi-domain proteins involved in diverse cellular processes. In fibroblasts, GIT is thought to regulate focal adhesion (FA) turnover, cell spreading, and motility through interaction with various proteins. In T lymphocytes, GIT interacts with PIX (Pak-interacting Rac/Cdc42 guanine exchange factor) and PAK (p21-activated kinase) and forms a trimolecular complex. Our understanding of the physiological roles of GIT in T cells is very limited. To determine the role of GIT1 and GIT2 in vivo, we generated GIT1- and GIT2- deficient mice. GIT1 is highly expressed in the brain, heart and testes. GIT2 is the major isoform expressed in hematopoietic cells. We found that GIT1 deficiency increased lethality, leading to perinatal death within 1-2 days after birth with a defect in brain development. GIT2-deficient mice were born healthy at normal Mendelian ratios. Interestingly, GIT2-deficient splenic T cells showed increased basal and chemokine-dependent migration. Furthermore, immature double positive thymocytes from GIT2-deficient mice showed increased basal and chemokine-induced migration. Since migration of thymocytes in the thymus has been tightly linked to their development, we crossed these mice to TCR transgenic mouse lines to better define the alterations in T-cell development and function by limiting compensation by repertoire selection. We found that the transition from the CD4 and CD8 double positive stage to CD4 single positive stage was greatly inhibited in the thymus of TCR transgenic GIT2-deficient mice. We are currently testing the hypothesis that GIT2 deficient-thymocytes have an altered migratory behavior leading to a defect in CD4 single positive thymocyte development. *H.P. is supported by the Leukemia and Lymphoma Society Special Fellow Award.

15

Shahraki, Abdolrazagh Hashemi, Subba Rao Chaganti, and Daniel Heath. "Assessing high-throughput environmental DNA extraction methods for meta-barcode characterization of aquatic microbial communities." Journal of Water and Health 17, no. 1 (October 30, 2018): 37–49. http://dx.doi.org/10.2166/wh.2018.108.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Abstract The characterization of microbial community dynamics using genomic methods is rapidly expanding, impacting many fields including medical, ecological, and environmental research and applications. One of the biggest challenges for such studies is the isolation of environmental DNA (eDNA) from a variety of samples, diverse microbes, and widely variable community compositions. The current study developed environmentally friendly, user safe, economical, and high throughput eDNA extraction methods for mixed aquatic microbial communities and tested them using 16 s rRNA gene meta-barcoding. Five different lysis buffers including (1) cetyltrimethylammonium bromide (CTAB), (2) digestion buffer (DB), (3) guanidinium isothiocyanate (GITC), (4) sucrose lysis (SL), and (5) SL-CTAB, coupled with four different purification methods: (1) phenol-chloroform-isoamyl alcohol (PCI), (2) magnetic Bead-Robotic, (3) magnetic Bead-Manual, and (4) membrane-filtration were tested for their efficacy in extracting eDNA from recreational freshwater samples. Results indicated that the CTAB-PCI and SL-Bead-Robotic methods yielded the highest genomic eDNA concentrations and succeeded in detecting the core microbial community including the rare microbes. However, our study recommends the SL-Bead-Robotic eDNA extraction protocol because this method is safe, environmentally friendly, rapid, high-throughput and inexpensive.

16

Haratua Gultom, Chandra S., R. Madhakomala, and Hamidah. "Evaluation Of The Effectiveness Of The Initial Flight Attendant Training Program In Garuda Indonesia Training Center." Journal of Business and Behavioural Entrepreneurship 4, no. 2 (December 21, 2020): 47–65. http://dx.doi.org/10.21009/jobbe.004.2.05.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

The purpose of this study is to evaluate the training effectiveness on GITC by applying the four levels Kirkpatrick model consisting of reaction, learning, behavior & Results. This study is cross sectional, primary data was collected through interviews from different batches representing different levels of the Kirkpatrick model. Effectiveness of training at the different levels was being evaluated through construct/theme developed on the basis of literature review. For level one evaluation interviews were conducted from employees who had recently completed their training; for level 2,3&4 the respondents, who had completed same training about 3 months, 6 months and year earlier respectively. The results indicated that reaction of the participants were positive for training except duration was too short, secondly they have applied skills & knowledge which they had learnt from training. A positive consequence of the training is that most of the participants got promoted from their current designation with the improvement in their pay scales. Thus, the soft skills trainings were effective with the participants desiring more opportunities to attend soft skills training session at least quarterly basis, to further improve their skills and enhance their knowledge.

17

Abdulla, Ahmed R., Ali H. Mohammed Ali, Khudair J. Al-Rawaq, and Anas N. Ibraheem. "IL-10 serum level estimation in Iraqi colorectal and gastric cancer patients." Journal of the Faculty of Medicine Baghdad 54, no. 2 (July 1, 2012): 167–71. http://dx.doi.org/10.32007/jfacmedbagdad.542750.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Background:Gastrointestinal cancers (GITc) is a worldwide problem. In Iraq , Gastric cancer is the 9th commonest of the top cancers while colorectal cancers it is considered as the 7th commonest ten cancers.IL-10 appears to be more of a pro-tumor than anti-tumor properties in both colorectal and gastric cancers.Objective:is to estimate the serum level of IL-10 in the Iraqi colorectal and gastric cancer Patientsand its relation to the progress of disease.Patients and Methods:In ourstudy ,54 serum samples werecollected starting from the 1st of January to mid of March 2011, to investigate the IL-10 serum level by using ELISA kit. 38colorectal and gastric cancer patients (H.Pylori +ve) and 16 of healthy control group.Results: The results showed that IL-10 serum levels of both GIT tumors were increased significantly (p<0.05) comparing with the healthy control group.Conclusion:In conclusion, the high serum level of IL-10 in colorectal cancers is due to the pro-tumor properties of IL-10 while in gastric cancer while the association of IL-10 genotypes specifically the single nucleotide polymorphism of the IL-10 promoter region may be the source of its serum increasing level.

18

Wibawanti, Retno, Amilya Agustina, and Retno Asti Werdhani. "Development of FRAMES (Fatigue Risk Assessment with Medical Advise) Application: Self-Assessment Application for Pilots." Indonesian Journal of Community and Occupational Medicine 2, no. 3 (March 29, 2023): 132–5. http://dx.doi.org/10.53773/ijcom.v2i3.71.132-5.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Introduction: Pilots have job characteristics that are at risk of causing fatigue. Since fatigue is not a disease, it is important to manage the risk factors. We developed a self-assessment application to manage the fatigue risk for pilots, including physical activity and sleeping difficulties. This application aims to increase pilots’ awareness as one of the health maintenance measures.Methods: The application was developed in collaboration with Garuda Indonesia Training Centre (GITC) to ensure suitable educational content for pilots. The users were asked to fill in data inquiring about their flight characteristics, the Checklist Individual Strength-20 for fatigue screening, General Physical Activity Questionnaire for physical activity, and Jenkins Sleep Scale for sleep difficulties. Afterward, a recommendation will be given based on the received input.Results: The application was able to screen fatigue risks, physical activities, and sleeping difficulties, and provide recommendations based on the questionnaire that was filled in, all adjusted to the user’s work characteristics. The finalized version was then available for download as an Android-based application for the pilots in GITC.Conclusion: The FRAMES is an Android-based self-assessment application for pilots. With the use of this application, hopefully, fatigue can be detected early in pilots, hence counteract measures may be implemented sooner to mitigate fatigue.

19

Sun, Shuping, Luqin Si, Zhaoze Fan, Jun Qiu, and Gao Li. "Stereoselective HPLC assay of TJ0711 enantiomers by precolumn derivatization with GITC using UV detection and its application in pharmacokinetics in rats." Journal of Huazhong University of Science and Technology [Medical Sciences] 29, no. 4 (August 2009): 427–30. http://dx.doi.org/10.1007/s11596-009-0407-7.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

20

Byrne, S. M., and C. S. Hoffman. "Six git genes encode a glucose-induced adenylate cyclase activation pathway in the fission yeast Schizosaccharomyces pombe." Journal of Cell Science 105, no. 4 (August 1, 1993): 1095–100. http://dx.doi.org/10.1242/jcs.105.4.1095.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

An important eukaryotic signal transduction pathway involves the regulation of the effector enzyme adenylate cyclase, which produces the second messenger, cAMP. Previous genetic analyses demonstrated that glucose repression of transcription of the Schizosaccharomyces pombe fbp1 gene requires the function of adenylate cyclase, encoded by the git2 gene. As mutations in git2 and in six additional git genes are suppressed by exogenous cAMP, these ‘upstream’ git genes were proposed to act to produce a glucose-induced cAMP signal. We report here that assays of cAMP levels in wild-type and various mutant S. pombe cells, before and after exposure to glucose, show that this is the case. The data suggest that the cAMP signal results from the activation of adenylate cyclase. Therefore these ‘upstream’ git genes appear to encode a glucose-induced adenylate cyclase activation pathway. Assays of cAMP on a strain carrying a mutation in the git6 gene, which acts downstream of adenylate cyclase, indicate that git6 may function to feedback regulate adenylate cyclase activity. Thus git6 may encode a cAMP-dependent protein kinase.

21

Nishi, Hiroyuki, Tsukasa Fukuyama та Masaaki Matsuo. "Resolution of optical isomers of 2,3,4,6-tetra-O-acetyl-β-D-glucopyranosyl isothiocyanate (GITC)-derivatized DL-amino acids by micellar electrokinetic chromatography". Journal of Microcolumn Separations 2, № 5 (вересень 1990): 234–40. http://dx.doi.org/10.1002/mcs.1220020506.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

22

KIKURA, RURI, AKIKO ISHIGAMI, and YUJI NAKAHARA. "Studies on Comparison of Metabolites in Urine between Deprenyl and Methamphetamine. III. Enantiomeric Composition Analysis of Metabolites in Mouse Urine by HPLC with GITC Chiral Reagent." Eisei kagaku 38, no. 2 (1992): 136–41. http://dx.doi.org/10.1248/jhs1956.38.136.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

23

Ezeanosike, Obumneme B., and Onyenmechi J. Afonne. "Prognostic significance of micro RNA 150 marker in BCR-ABL positive chronic myeloid leukaemia patients on imatinib mesylate." International Journal of Contemporary Pediatrics 4, no. 5 (August 23, 2017): 1557. http://dx.doi.org/10.18203/2349-3291.ijcp20173763.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Background: Micro-RNAs control gene expression by destabilizing targeted transcripts and inhibiting their translation. In chronic myeloid leukaemia (CML), abnormal expressions of miRNAs have been described. The current treatment for newly diagnosed cases of CML is imatinib mesylate which produces rapid haematological responses. It is currently impossible to predict whether a patient will develop resistance to imatinib mesylate. This makes identification of predictors of resistance to imatinib an important goal in management of patients with CML. MicroRNA expression patterns can be used to predict outcome which can be remission or relapse. This study therefore, was set to assess the possible use of microRNA 150 for prognostication.Methods: Fifty peripheral blood samples previously collected from CML patients who were being treated with imatinib mesylate and stored in the refrigerator at +4°C were analyzed for the expression of microRNAs 150. Total RNA was extracted from guanidium isothiocynate (GITC) lysate of the blood samples using RNeasy mini spin column. The total RNA was converted to complimentary DNA by random hexamer priming using Murine Moloney Leukaemia Virus Reverse Transcriptase. Real time Multiplex PCR was used for detecting Breakpoint Cluster Region-Abelson Murine Leukaemia (BCR-ABL) transcript type.Results: The patients’ samples showed an expression of miRNA-150. Correlation of BCR-ABL ratio with miRNA-150 was done and the Spearman correlation coefficient (Rho) between BCR-ABL1 and miRNA-150 was 0.442 (p = 0.001; CI = 0.18-0.65) showing that there was a positive correlation between BCR-ABL1 and miRNA-150. The coefficient of determination was 20% (CI = 3-42%), which implies that about 20% of BCR-ABL1 ratio could be accounted for by the miRNA-150 values.Conclusions: Therefore, once patients who are on imatinib achieve molecular remission of the CML, the miRNA-150 can be useful in predicting outcome which could be relapse or complete molecular remission but is weak at diagnosis in predicting such outcome.

24

Ivey, F. Douglas, Francis X. Taglia, Fan Yang, Matthew M. Lander, David A. Kelly та Charles S. Hoffman. "Activated Alleles of the Schizosaccharomyces pombegpa2+ Gα Gene Identify Residues Involved in GDP-GTP Exchange". Eukaryotic Cell 9, № 4 (5 лютого 2010): 626–33. http://dx.doi.org/10.1128/ec.00010-10.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

ABSTRACT The Schizosaccharomyces pombe glucose/cyclic AMP (cAMP) signaling pathway includes the Gpa2-Git5-Git11 heterotrimeric G protein, whose Gpa2 Gα subunit directly binds to and activates adenylate cyclase in response to signaling from the Git3 G protein-coupled receptor. To study intrinsic and extrinsic regulation of Gpa2, we developed a plasmid-based screen to identify mutationally activated gpa2 alleles that bypass the loss of the Git5-Git11 Gβγ dimer to repress transcription of the glucose-regulated fbp1 + gene. Fifteen independently isolated mutations alter 11 different Gpa2 residues, with all but one conferring a receptor-independent activated phenotype upon integration into the gpa2 + chromosomal locus. Biochemical characterization of three activated Gpa2 proteins demonstrated an increased GDP-GTP exchange rate that would explain the mechanism of activation. Interestingly, the amino acid altered in the Gpa2(V90A) exchange rate mutant protein is in a region of Gpa2 with no obvious role in Gα function, thus extending our understanding of Gα protein structure-function relationships.

25

Greenberg, Daniel L., and Alex Spencer. "Complex and Novel Associations of the Guanine Exchange Factors Cool- 1 and Cool-2 with the Scaffolding Proteins GIT1 and GIT2 in Human Platelets." Blood 112, no. 11 (November 16, 2008): 2870. http://dx.doi.org/10.1182/blood.v112.11.2870.2870.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Abstract A major signaling pathway that regulates platelet shape change and reorganization of the cytoskeleton involves the Rho family of GTPases; CDC42 (fillapodia), Rac1 (lamellapodia) and RhoA (focal adhesions). These GTPases are converted from their inactive or GDP-loaded state to the active or GTP-loaded state by a class of enzymes called Guanine Exchange Factors (GEFs). GEFs are a family of multi-domain proteins that contain a GDP-GTP exchange domain (DH-PH) as well as other protein interacting domains that are regulated by the activation of receptors present on the platelet surface. We used an affinity binding technique followed by mass spectroscopy to identify novel Rho family binding GEFs in platelet lysates. Recombinant GST-Rho fusion proteins bound to agarose beads were prepared in the GTP, GDP and nucleotide-free states and incubated with clarified human platelet lysates. Platelet lysate proteins associated with the different GST-Rho preparations were eluted and run on SDS-PAGE. Gel slices were then cut out, trypsin digested and analyzed by Mass Spectroscopy. Platelet GEFs were identified by the presence of a DH-PH domain. Using this technique we found Cool-1 and Cool-2, two closely related GEFs that regulate Rac1 and CDC42 activation in nucleated cells. Cool-1 has not been previously described in platelets. Homodimeric Cool-1 specifically activates CDC42, whereas Cool-2 is capable of activating Rac1 as a homodimer or CDC42 as a monomer. The substrate specificity of Cool-2 is regulated by complex interactions with p21-activated kinases (PAK) and Gb/g proteins. In nucleated cells, Cool-1 and Cool-2 are localized to focal adhesions by the GPCR-kinase-interacting proteins 1 and 2 (GIT1 and GIT2). GIT binding to the Cool proteins has been shown to inhibit their GEF activity. Here we show that Cool-1 is present only in the membrane fraction of resting platelet lysates while Cool-2 is present in both the membrane and cytoplasmic fractions. Upon activation with thrombin, about half the membrane bound Cool-1 and all the membrane bound Cool- 2 migrate to the cytoplasm. Precipitation experiments in thrombin activated platelets with anti-GIT1 and anti-GIT2 antibodies show GIT-1 avidly binds Cool-2 whereas GIT2 binds a small amount of Cool-1. These data suggest a complex mechanism of CDC42 and Rac1 activation in platelets by the Cool proteins. Based on our findings and the current understanding of the regulation of Cool proteins in nucleated cells, we hypothesize that early after thrombin activation, the CDC42 and Rac1 GEF activities of Cool-1 and Cool-2 result in fillapodia (CDC42) and lamellapodia (Rac1) formation. As integrant mediated focal adhesions are formed, the GEF activities of Cool-1 and Cool-2 are inhibited by the scaffolding proteins GIT2 and GIT1, respectively. In this manner, Rac1 and CDC42 mediated fillapodia and lamellapodia formation may be regulated by the extent of integrin engagement and platelet spreading.

26

Shikata, Yasushi, Konstantin G. Birukov, and Joe G. N. Garcia. "S1P induces FA remodeling in human pulmonary endothelial cells: role of Rac, GIT1, FAK, and paxillin." Journal of Applied Physiology 94, no. 3 (March 1, 2003): 1193–203. http://dx.doi.org/10.1152/japplphysiol.00690.2002.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Sphingosine 1-phosphate (S1P) enhances human pulmonary endothelial monolayer integrity via Rac GTPase-dependent formation of a cortical actin ring (Garcia et al. J Clin Invest 108: 689–701, 2001). The mechanisms underlying this response are not well understood but may involve rapid redistribution of focal adhesions (FA) as attachment sites for actin filaments. We evaluate the effects of S1P on the redistribution of paxillin, FA kinase (FAK), and the G protein-coupled receptor kinase-interacting proteins (GITs). S1P induced Rac GTPase activation and cortical actin ring formation at physiological concentrations (0.5 μM), whereas 5 μM S1P caused prominent stress fiber formation and activation of Rho and Rac GTPases. S1P (0.5 μM) stimulated the tyrosine phosphorylation of FAK Y576, and paxillin was linked to FA disruption and redistribution to the cell periphery. Furthermore, S1P induced a transient association of GIT1 with paxillin and redistribution of the GIT2-paxillin complex to the cell cortical area without affecting GIT2-paxillin association. These results suggest a role of FA rearrangement in S1P-mediated barrier enhancement via Rac- and GIT-mediated processes.

27

Reese, William D. "Gemmipars in the Calymperaceae." Bryologist 104, no. 2 (June 2001): 299–302. http://dx.doi.org/10.1639/0007-2745(2001)104[0299:gitc]2.0.co;2.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

28

Tritz, Céline, Sylvain Bigot, Sandra Rome, Léa David, Isabelle Pochelon, and Sophie Schiavone. "Perception du changement climatique et de ses impacts sur les activités touristiques: exemple d’une enquête exploratoire dans le département de la Drôme (sud-est de la France)." Géo-Regards 5, no. 1 (2012): 111–25. http://dx.doi.org/10.33055/georegards.2012.005.01.111.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Le tourisme est une des activités dont l’économie est très dépendante des variations du climat, à travers, par exemple des ambiances thermiques favorables, ou encore des chutes de neige en quantité et en qualité suffisante permettant la pratique des activités d’hiver. Afin d’établir un diagnostic précis des évolutions climatiques aujourd’hui avérées (GIEC, 2007) et de leurs influences sur les attentes des professionnels du milieu touristique (hébergeurs, restaurateurs, institutionnels…) à travers leurs perceptions, une enquête électronique a été menée au sein du département de la Drôme auprès de 2 404 acteurs recensés pour leur appartenance au secteur du tourisme. Cette étude est effectuée dans le cadre du programme de recherche DECLIC (Drôme : Eau, Climat et Impacts liés aux Changements) mené en collaboration avec le Conseil général de la Drôme, et inscrit dans le programme national GICC-2 (Gestion et Impacts du Changement Climatique) du MEEDDM (ministère français de l’Environnement et du Développement durable)

29

Regnauld, Hervé. "GIEC." L'Information géographique Vol. 85, no. 1 (March 15, 2021): 89–93. http://dx.doi.org/10.3917/lig.851.0089.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

30

Ephrem, Amal, Alan Epstein, and Ethan Shevach. "The Glucocorticoid-Induced Tumor necrosis-factor related Receptor (GITR) is a redundant costimulatory molecule for conventional T (Tconv) cells and plays a dual role on Regulatory T cells (Treg). (179.17)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 179.17. http://dx.doi.org/10.4049/jimmunol.188.supp.179.17.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Abstract Treg control immune homeostasis, but are also responsible for the suppression of tumor immunity; thus, reversing Treg function is a promising strategy for cancer therapy. The GITR is highly expressed on Treg, and upregulated on Tconv after activation. The GITR-L is primarily expressed on APC. Manipulation of GITR/GITR-L interactions in vivo has resulted in enhancement of immune responses, but whether the enhancement is secondary to co-stimulation of Tconv or reversal of Treg-mediated suppression remains unclear. To resolve this controversy, we used GITR-/- and GITR-L-/- mice and Fc-GITR-L in several experimental models. Treatment of mice with Fc-GITR-L induced the expansion of Treg. Polyclonal GITR-/- Treg survived less well than WT Treg following transfer to normal mice suggesting that GITR/GITR-L interactions are important for the survival of Tconv. In contrast, the expansion of both antigen-specific WT Tconv and Treg was not impaired following transfer to GITR-L-/- recipients. Although the capacity of GITR-/- Treg to suppress IBD was similar to WT, injection of GITR-L exacerbated IBD in mice that received CD45RBhigh T cells and in mice that received and CD45RBhigh cells and Treg. GITR-L treatment in this latter group resulted in a loss of Foxp3 expression. Thus, the GITR is a redundant molecule for costimulation of Tconv, but engagement of the GITR on Treg can result in different outcomes (expansion or loss of Foxp3) depending on the nature of the immune stimulus.

31

Hasi, Rumana Yesmin, Makoto Miyagi, Katsuya Morito, Toshiki Ishikawa, Maki Kawai-Yamada, Hiroyuki Imai, Tatsuya Fukuta, et al. "Glycosylinositol phosphoceramide-specific phospholipase D activity catalyzes transphosphatidylation." Journal of Biochemistry 166, no. 5 (August 26, 2019): 441–48. http://dx.doi.org/10.1093/jb/mvz056.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Abstract Glycosylinositol phosphoceramide (GIPC) is the most abundant sphingolipid in plants and fungi. Recently, we detected GIPC-specific phospholipase D (GIPC-PLD) activity in plants. Here, we found that GIPC-PLD activity in young cabbage leaves catalyzes transphosphatidylation. The available alcohol for this reaction is a primary alcohol with a chain length below C4. Neither secondary alcohol, tertiary alcohol, choline, serine nor glycerol serves as an acceptor for transphosphatidylation of GIPC-PLD. We also found that cabbage GIPC-PLD prefers GIPC containing two sugars. Neither inositol phosphoceramide, mannosylinositol phosphoceramide nor GIPC with three sugar chains served as substrate. GIPC-PLD will become a useful catalyst for modification of polar head group of sphingophospholipid.

32

Setyaningsih and Heny Perbowosari. "PEMBENTUKAN SIKAP RELIGIUS ANAK MELALUI PEMBACAAN SLOKA BHAGAWADGITA DI PASRAMAN INDRAPRASTA." VIDYA SAMHITA: Jurnal Penelitian Agama 8, no. 1 (April 30, 2022): 39–46. http://dx.doi.org/10.25078/vs.v8i1.939.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Bhagawad Gita artinya Nyanyian atau sabda Tuhan Yang Maha Esa. Gita adalah rangkuman musik, rangkuman dari berbagai nada dalam satu kesatuan yang indah. Didalam Bhagawad Gita terpancar adanya sebuah filsafat yang mengalir dalam bentuk, sebuah lagu, dan merupakan susunan sloka-sloka (syair-syair) filsafat kehidupan nan paling agung dalam seni sastra dunia. Adapun tujuan dari penelitian ini antara lain untuk menganalisis wujud implementasi ajaran Bhagawad Gita dalam membentuk karakter siswa pasraman Indraprasta, cara dan teknik membaca sloka Bhagawad Gita, serta manfaat bagi peserta didik setelah pembacaan sloka. Bhagawad Gita dikenal sebagai mutiara pengetahuan rohani. Bhagawad Gita berisi ajaran-ajaran suci yang dapat mengupas tentang penekanan-penekanan hidup. Bhagawad Gita diperlukan sebagai penuntun hidup untuk memperbaiki sikap dan moral kita, karena Bhagawad Gita tidak hanya mengajarkan tentang konsep ketuhanan, artha, dharma, kama, maupun moksa. Bhagawad Gita juga mengajarkan tentang tuntunan kehidupan, kemanusiaan, dan moralitas, keberadaan pasraman Indraprasta, Mutihan Sondakan, Kecamatan Laweyan,Surakarta dapat mengubah karakter para peserta didik melalui pembiasaan membaca sloka Bhagawad Gita. Program tersebut mampu mewujudkan para peserta didik menjadi lebih religious, disiplin, semangat dalam belajar menguasai sloka Bhagawad Gita, para siswa dibiasakan untuk membiasakan membaca sloka Bhagawad Gita maka akan terbentuk kebiasaan – kebiasaan yang baik, karena di dalam Bhagawad Gita mengandung nilai-nilai yang dapat merubah karakter siswa dan meningkatkan ajaran spiritual para peserta didik sejak dini. Kata Kunci : Pembiasaan, Pembacaan Sloka, Religius

33

Chan, Sarah, Nicole Belmar, Sun Ho, Bryan Rogers, Marcia Stickler, Michelle Graham, Eileen Lee, et al. "An anti-PD-1–GITR-L bispecific agonist induces GITR clustering-mediated T cell activation for cancer immunotherapy." Nature Cancer 3, no. 3 (March 2022): 337–54. http://dx.doi.org/10.1038/s43018-022-00334-9.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

AbstractCostimulatory receptors such as glucocorticoid-induced tumor necrosis factor receptor–related protein (GITR) play key roles in regulating the effector functions of T cells. In human clinical trials, however, GITR agonist antibodies have shown limited therapeutic effect, which may be due to suboptimal receptor clustering-mediated signaling. To overcome this potential limitation, a rational protein engineering approach is needed to optimize GITR agonist-based immunotherapies. Here we show a bispecific molecule consisting of an anti-PD-1 antibody fused with a multimeric GITR ligand (GITR-L) that induces PD-1-dependent and FcγR-independent GITR clustering, resulting in enhanced activation, proliferation and memory differentiation of primed antigen-specific GITR+PD-1+ T cells. The anti-PD-1–GITR-L bispecific is a PD-1-directed GITR-L construct that demonstrated dose-dependent, immunologically driven tumor growth inhibition in syngeneic, genetically engineered and xenograft humanized mouse tumor models, with a dose-dependent correlation between target saturation and Ki67 and TIGIT upregulation on memory T cells. Anti-PD-1–GITR-L thus represents a bispecific approach to directing GITR agonism for cancer immunotherapy.

34

Suvas, Susmit, Bumseok Kim, Pranita P. Sarangi, Masahide Tone, Herman Waldmann, and Barry T. Rouse. "In Vivo Kinetics of GITR and GITR Ligand Expression and Their Functional Significance in Regulating Viral Immunopathology." Journal of Virology 79, no. 18 (September 15, 2005): 11935–42. http://dx.doi.org/10.1128/jvi.79.18.11935-11942.2005.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

ABSTRACT This report evaluates the role of interaction between glucocorticoid-induced tumor necrosis factor receptor (GITR) and GITR ligand (GITR-L) in the immunoinflammatory response to infection with herpes simplex virus (HSV). Both GITR and GITR-L were transiently upregulated after ocular HSV infection, on antigen-specific T cells and antigen-presenting cells, respectively, in the draining lymph node (DLN). In addition, virus-specific T-cell responses in the DLN and spleen were enhanced by anti-GITR antibody treatment, an outcome expected to result in more severe inflammatory lesions. Intriguingly, the treatment resulted in significantly diminished T-cell-mediated ocular lesions. The explanation for these findings was that anti-GITR antibody treatment caused a reduced production of ocular MMP-9, a molecule involved in ocular angiogenesis, an essential step in the pathogenesis of herpetic keratitis. Our results are the first observations to determine in vivo kinetics of GITR and GITR-L expression after virus infection, and they emphasize the role of GITR-GITR-L interaction to regulate virus-induced immunoinflammatory lesions.

35

Liao, Gongxian, Scott Berger, Cynthia Detre, Rene de Waal Malefyt, Roland Herzog, Atul Bhan, and Cox Terhorst. "GITR on the surface of antigen presenting cells, but not on T cells, regulates the pathogenesis of CD4+ T cell-mediated experimental colitis (120.3)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 120.3. http://dx.doi.org/10.4049/jimmunol.188.supp.120.3.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Abstract The receptor GITR is thought to function on the surface of regulatory and activated effector CD4+ T cells. To better understand the role of GITR in in vivo immune responses, we use an established experimental colitis model. Chronic enterocolitis was induced by the transfer of wt or GITR−/− CD4+ T cells into either GITR−/− x Rag−/− or Rag−/− recipients. When non-fractionated CD4+ cells from either wt or GITR−/− donors were transferred, colitis unexpectedly developed in GITR−/− x Rag−/−, but not in Rag−/− recipients. In these mice, the percentage of Treg and Th17 cells is decreased, whilst that of Th1 cells increased. Furthermore, Tregs fail to prevent colitis in GITR−/− x Rag−/− recipients. This is not due to an aberrant function of GITR−/− Treg or Teff cells, but is caused by an imbalance in the number of tolerogenic CD103+ and PDCA1+ plasmacytoid dendritic cells in the GITR−/− mouse. This in turn impairs Treg development and expands the Th1 population in GITR−/− x Rag−/− recipients upon the transfer of non-fractionated CD4+ cells. We conclude that for the induction of colitis, GITR is dispensable on the surface of Treg and Teff cells, nor do GITR-L / GITR interactions on T cells play a role in controlling the disease. GITR, however, controls in vivo DC and monocyte development and in its absence aggravated chronic enterocolitis is caused by an imbalance of colitogenic Th1 cells and regulatory T cells.

36

Totaro, Antonio, Simona Paris, Claudia Asperti, and Ivan de Curtis. "Identification of an Intramolecular Interaction Important for the Regulation of GIT1 Functions." Molecular Biology of the Cell 18, no. 12 (December 2007): 5124–38. http://dx.doi.org/10.1091/mbc.e07-06-0550.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

G-protein coupled receptor kinase-interacting protein (GIT) proteins include an N-terminal Arf GTPase-activating protein domain, and a C terminus that binds proteins regulating adhesion and motility. Given their ability to form large molecular assemblies, the GIT1 protein must be tightly regulated. However, the mechanisms regulating GIT1 functions are poorly characterized. We found that carboxy-terminal–truncated fragments of GIT1 bind their partners with higher efficiency compared with the full-length GIT1. We have explored the hypothesis that GIT1 is regulated by an intramolecular mechanism, and we identified two distinct intramolecular interactions between the N and C terminus of GIT1. The release of these interactions increases binding of GIT1 to paxillin and liprin-α, and it correlates with effects on cell spreading. Analysis of cells plated on fibronectin has shown that different deletion mutants of GIT1 either enhance or inhibit spreading, depending on their subcellular localization. Moreover, although the association between βPIX and GIT1 is insufficient to activate GIT1 binding to paxillin, binding of a PAK1 fragment including the βPIX-binding domain enhances paxillin binding to βPIX/GIT1, indicating that p21-activated kinase can activate the binding of paxillin to GIT1 by a kinase-independent mechanism. The release of the identified intramolecular interaction seems to be an important mechanism for the regulation of GIT1 functions.

37

Lou, Xiaojing, Hiroko Yano, Francis Lee, Moses V. Chao, and Marilyn Gist Farquhar. "GIPC and GAIP Form a Complex with TrkA: A Putative Link between G Protein and Receptor Tyrosine Kinase Pathways." Molecular Biology of the Cell 12, no. 3 (March 2001): 615–27. http://dx.doi.org/10.1091/mbc.12.3.615.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

NGF initiates the majority of its neurotrophic effects by promoting the activation of the tyrosine kinase receptor TrkA. Here we describe a novel interaction between TrkA and GIPC, a PDZ domain protein. GIPC binds to the juxtamembrane region of TrkA through its PDZ domain. The PDZ domain of GIPC also interacts with GAIP, an RGS (regulators of G protein signaling) protein. GIPC and GAIP are components of a G protein-coupled signaling complex thought to be involved in vesicular trafficking. In transfected HEK 293T cells GIPC, GAIP, and TrkA form a coprecipitable protein complex. Both TrkA and GAIP bind to the PDZ domain of GIPC, but their binding sites within the PDZ domain are different. The association of endogenous GIPC with the TrkA receptor was confirmed by coimmunoprecipitation in PC12 (615) cells stably expressing TrkA. By immunofluorescence GIPC colocalizes with phosphorylated TrkA receptors in retrograde transport vesicles located in the neurites and cell bodies of differentiated PC12 (615) cells. These results suggest that GIPC, like other PDZ domain proteins, serves to cluster transmembrane receptors with signaling molecules. When GIPC is overexpressed in PC12 (615) cells, NGF-induced phosphorylation of mitogen-activated protein (MAP) kinase (Erk1/2) decreases; however, there is no effect on phosphorylation of Akt, phospholipase C-γ1, or Shc. The association of TrkA receptors with GIPC and GAIP plus the inhibition of MAP kinase by GIPC suggests that GIPC may provide a link between TrkA and G protein signaling pathways.

38

Xu, Runze, Ran Xu, Yuanxiang Wang, Weixing Wang, Lingling Jiang, and Shishun Gong. "G-Protein-Coupled Receptor Kinase-Interacting Protein 1 (GIT1) Promotes Head and Neck Squamous Cell Carcinoma Metastases via Activating the PI3K/AKT/mTOR Signal Pathway." Computational and Mathematical Methods in Medicine 2022 (January 25, 2022): 1–9. http://dx.doi.org/10.1155/2022/6881932.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Objective. GIT1 is identified as a novel tumor oncogene in breast cancer. In this article, we aimed to explore the role of GIT1 in the progression of head and neck squamous cell carcinoma (HNSCC). Methods. GIT1 expression in HNSCC was detected by RT-qPCR, immunohistochemistry assay, and Western blot. HNSCC cell proliferation, migration, and invasion were examined by CCK-8 assay, Wound healing assay, and Transwell assay, respectively. Cell apoptosis was detected by flow cytometric analysis. Results. In our study, GIT1 was notably upregulated in HNSCC tissues and cells. Moreover, GIT1 expression level had positive corelation with pathological grade and nodal status of HNSCC. Functional experiments showed that knockdown of GIT1 restrained HNSCC proliferation, invasion, migration, and EMT and facilitated cell apoptosis. Furthermore, GIT1 knockdown was found to restrain HNSCC tumor growth and lung metastasis. Additionally, PI3K/AKT/mTOR signal pathway inhibitors suppressed the effect of GIT1 on HNSCC cell progression. Conclusion. GIT1 was upregulated in HNSCC and facilitated HNSCC cell progression by inducing PI3K/AKT/mTOR signal pathway. Therefore, we suggested that GIT1 might be a potential target for HNSCC treatment.

39

Murphy, Judith, Taha Merghoub, Alan Houghton, and Jedd Wolchok. "A role for the GITR pathway in anaphylaxis (P4326)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 45.11. http://dx.doi.org/10.4049/jimmunol.190.supp.45.11.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Abstract Immune modulation using monoclonal antibodies has a significant impact on the overall survival of patients with metastatic melanoma. Monoclonal antibodies that engage members of the tumor necrosis factor receptor (TNFR) superfamily have shown promising tumor protection in preclinical models. Glucocorticoid-induced TNFR-related protein (GITR) is a particularly potent target for tumor immunotherapy. A single dose of GITR agonist antibody results in 60% protection from established B16 melanoma tumors. Therefore, several doses of anti-GITR may be necessary in order to fully eradicate established tumors. Because GITR is expressed throughout the immune system, we investigated whether multiple doses of anti-GITR result in adverse immune-related events. We observed that three doses of anti-GITR cause anaphylaxis, a side effect that has not been reported using this or other TNFR superfamily agonist antibodies. Anaphylaxis was not observed upon the first or second doses of anti-GITR or in GITR knockout mice. Anti-GITR-induced anaphylaxis is associated with a severe drop in body temperature and elevated serum proinflammatory cytokine levels. We are further investigating the causes of toxicity resulting from repetitive anti-GITR treatment and whether this effect can be reversed or prevented while preserving the antitumor activity of anti-GITR, an important step given the translational potential of this therapy.

40

Mazaki, Yuichi, Shigeru Hashimoto, Katsuya Okawa, Asako Tsubouchi, Kuniaki Nakamura, Ryohei Yagi, Hajime Yano, et al. "An ADP-Ribosylation Factor GTPase-activating Protein Git2-short/KIAA0148 Is Involved in Subcellular Localization of Paxillin and Actin Cytoskeletal Organization." Molecular Biology of the Cell 12, no. 3 (March 2001): 645–62. http://dx.doi.org/10.1091/mbc.12.3.645.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Paxillin acts as an adaptor protein in integrin signaling. We have shown that paxillin exists in a relatively large cytoplasmic pool, including perinuclear areas, in addition to focal complexes formed at the cell periphery and focal adhesions formed underneath the cell. Several ADP-ribosylation factor (ARF) GTPase-activating proteins (GAPs; ARFGAPs) have been shown to associate with paxillin. We report here that Git2-short/KIAA0148 exhibits properties of a paxillin-associated ARFGAP and appears to be colocalized with paxillin, primarily at perinuclear areas. A fraction of Git2-short was also localized to actin-rich structures at the cell periphery. Unlike paxillin, however, Git2-short did not accumulate at focal adhesions underneath the cell. Git2-short is a short isoform of Git2, which is highly homologous to p95PKL, another paxillin-binding protein, and showed a weaker binding affinity toward paxillin than that of Git2. The ARFGAP activities of Git2 and Git2-short have been previously demonstrated in vitro, and we provided evidence that at least one ARF isoform, ARF1, is an intracellular substrate for the GAP activity of Git2-short. We also showed that Git2-short could antagonize several known ARF1-mediated phenotypes: overexpression of Git2-short, but not its GAP-inactive mutant, caused the redistribution of Golgi protein β-COP and reduced the amounts of paxillin-containing focal adhesions and actin stress fibers. Perinuclear localization of paxillin, which was sensitive to ARF inactivation, was also affected by Git2-short overexpression. On the other hand, paxillin localization to focal complexes at the cell periphery was unaffected or even augmented by Git2-short overexpression. Therefore, an ARFGAP protein weakly interacting with paxillin, Git2-short, exhibits pleiotropic functions involving the regulation of Golgi organization, actin cytoskeletal organization, and subcellular localization of paxillin, all of which need to be coordinately regulated during integrin-mediated cell adhesion and intracellular signaling.

41

Siti, Nyoman, Budi Koestoro, and I. Dewa Made Raka. "Development Of Video Media Instructional Bhagavad Gita In Religious High School Hindu Lampung." Vidyottama Sanatana: International Journal of Hindu Science and Religious Studies 2, no. 1 (May 31, 2018): 75. http://dx.doi.org/10.25078/ijhsrs.v2i1.516.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

<p>The objectives of this research are: (1) developing video media teaching materials of Bhagavad Gita, (2) to analyze the effectiveness of Bhagavad Gita video media use, (3) to analyze the efficiency of Bhagavad Gita video media, (4) to analyze the attractiveness of Bhagavad Gita video media. This research uses a research and development approach, conducted in religious high school hindu (STAH) Lampung. Data collection using tests and questionnaires and analyzed quantitatively and qualitatively. The conclusions of the study were (1) to produce teaching material of Bhagavad Gita video media consisting of eight elements, namely: (a) opening greetings, (b) introduction, (c) parts of Bhagavad Gita, (d) how to read, (e) types of mentrum, (f) examples, (g) self-assessment and (h) closing greetings. (2) video media teaching materials Bhagavad Gita effective with the average of the gain value in sequence is 0.71; 0.77; and 0.77. (3) Bhagavad Gita video media is efficient as a learning media of 1.7. (4) The video media instructional Bhagavad Gita is attractive in used as media video learning Bhagavad Gita with the consecutive average percentage being 91%, 91%, and 92%.</p>

42

Ronchetti, Simona, Erika Ricci, Maria Grazia Petrillo, Luigi Cari, Graziella Migliorati, Giuseppe Nocentini, and Carlo Riccardi. "Glucocorticoid-Induced Tumour Necrosis Factor Receptor-Related Protein: A Key Marker of Functional Regulatory T Cells." Journal of Immunology Research 2015 (2015): 1–17. http://dx.doi.org/10.1155/2015/171520.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Glucocorticoid-induced tumour necrosis factor receptor-related protein (GITR, TNFRSF18, and CD357) is expressed at high levels in activated T cells and regulatory T cells (Tregs). In this review, we present data from mouse and human studies suggesting that GITR is a crucial player in the differentiation of thymic Tregs (tTregs), and expansion of both tTregs and peripheral Tregs (pTregs). The role of GITR in Treg expansion is confirmed by the association of GITR expression with markers of memory T cells. In this context, it is not surprising that GITR appears to be a marker of active Tregs, as suggested by the association of GITR expression with other markers of Treg activation or cytokines with suppressive activity (e.g., IL-10 and TGF-β), the presence of GITR+cells in tissues where Tregs are active (e.g., solid tumours), or functional studies on Tregs. Furthermore, some Treg subsets including Tr1 cells express either low or no classical Treg markers (e.g., FoxP3 and CD25) and do express GITR. Therefore, when evaluating changes in the number of Tregs in human diseases, GITR expression must be evaluated. Moreover, GITR should be considered as a marker for isolating Tregs.

43

Davis, Andrew, Lori Cunningham, Matthew Stokes, Alissa Nelson, Kathryn Abell, Michael Lewis, Roy Scialdone, et al. "Phosphoproteomics reveals GITR agonism differentially regulates inflammatory vs. regulatory T cell subsets." Journal of Immunology 206, no. 1_Supplement (May 1, 2021): 57.15. http://dx.doi.org/10.4049/jimmunol.206.supp.57.15.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Abstract Triggering the co-stimulatory receptor glucocorticoid-induced TNFR-related protein (GITR) on T cells has been identified as a promising cancer immunotherapeutic strategy, yet the signaling events by which GITR agonism induces antitumor immunity are not well understood. GITR is expressed on activated CD4+ and CD8+ T cells, and is constitutively expressed on regulatory T cells (Tregs). While GITR appears to act as a conventional co-stimulatory receptor in effector CD4+ and CD8+ T cells, the role of GITR on Tregs remains controversial. The goal of this research was to utilize a phosphoproteomics approach to identify and compare GITR-mediated intracellular signaling events in induced-Tregs (iTregs), CD4+ T cells, and CD8+ cytotoxic T cells. We used the GITR agonist monoclonal antibody DTA-1 to stimulate the T cell subsets and confirmed GITR signaling via NFκB pathway activation and phospho-JNK induction. The phosphoproteomics data revealed different protein phosphorylation patterns among T cell subsets. For example, we observed phospho-p38 MAPK induction in the iTreg subset but not in the CD4+ T cells or CD8+ cytotoxic T cells. We also observed additional phospho-proteins induced by GITR triggering in the p38 pathway in the iTreg subset including phospho-MKK3, phospho-MKK6, phospho-MAPKAPK-2, and phospho-ATF-2. Induction of p38 MAPK signaling is functionally important as inhibition of p38 abrogated GITR-induced proliferation of iTregs. These data demonstrate that GITR agonism induces distinct phospho-proteome profiles between T cell subsets, and this differential signaling leads to unique responses that will need to be considered when targeting GITR with immunotherapeutic strategies.

44

Clouthier, Derek, Michael Wortzman, Angela Zhou, Olga Luft, Gary Levy, and Tania Watts. "The co-stimulatory molecule GITR intrinsically enhances type 1 and follicular helper CD4 T cell responses to establish early control of a persistent viral infection and potentiate the late humoral response (IRC9P.700)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 191.1. http://dx.doi.org/10.4049/jimmunol.192.supp.191.1.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Abstract During persistent infection, the immune system must be tightly regulated to balance immune control against pathology. The glucocorticoid-induced TNFR (GITR) is an important co-stimulatory molecule that plays a critical CD4 T cell-intrinsic role in the control of a mouse model of chronic viral infection, LCMV clone 13. 8 days post-infection (dpi) of wild-type (WT) and GITR-/- mice revealed that GITR-/- mice have 2-fold fewer LCMV-specific CD8 T cells, with higher PD-1 and Tim-3 levels. These defects became more striking at 45 dpi, when GITR-/- mice have a ~9-fold deficit in IFNγ+CD107+TNF+ CD8 T cells. GITR-/- mice had impaired viral control, with 35- and 10- fold higher viral load in the kidney at 8 and 45 dpi, respectively. Depletion of CD4 cells largely abrogated the differences between WT and GITR-/- mice at 8 dpi, suggesting that CD4 T cells underscore the impaired T cell responses of GITR-/- mice. GITR-/- mice have 3-4-fold fewer IFNγ+ and IL-2+ Th1 cells at 8 dpi. Using DEREG mice, we found that the compromised immunity and viral control in GITR-/- mice are independent of Foxp3+ Tregs. GITR-/- mice also had 2-fold fewer follicular helper (Tfh) cells at 21-45 dpi, with concomitant impairment in LCMV-specific IgG titres. Mixed bone marrow chimeras revealed a CD4 T cell-intrinsic role for GITR in potentiating Th1 and Tfh responses. Our findings reveal a critical role for GITR in co-stimulation of CD4 helper T cell subsets for optimal cell-mediated and humoral immunity.

45

Witomo, Cornelia Mirwantini, Nuddin Harahap, and Andi Kurniawan. "NILAI MANFAAT PARIWISATA EKOSISTEM TERUMBU KARANG TAMAN WISATA PERAIRAN GITA NADA SEKOTONG LOMBOK." Jurnal Sosial Ekonomi Kelautan dan Perikanan 15, no. 2 (December 30, 2020): 169. http://dx.doi.org/10.15578/jsekp.v15i2.9234.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Penelitian ini mengambarkan pola pemanfaatan pariwisata terumbu karang di Taman Wisata Perairan (TWP) Gita Nada dan mengestimasi nilai manfaat ekosistem terumbu karang dengan pendekatan biaya perjalanan sebagai dasar rujukan perencanaan pengembangan kawasan pariwisata di Kabupaten Lombok Barat. Penelitian dilakukan di Taman TWP Gita Nada Sekotong Lombok pada bulan Januari-Maret 2020. Pengumpulan data primer dilakukan dengan cara wawancara menggunakan kuisoner dan observasi segala aktivitas pariwisata yang ada di TWP Gita Nada. Data sekunder dikumpulkan dengan cara penelusuran literatur pada hasil penelitian terdahulu serta publikasi yang dilakukan oleh instansi terkait. Metode analisis yang digunakan adalah Zona Travel Cost Method (ZTCM). Perairan TWP Gita Nada memiliki kombinasi perairan dangkal dengan tipe fringing reefs dan letak TWP Gita Nada yang berbatasan dengan Selat Lombok. Atraksi wisata yang ditawarkan di TWP Gita Nada adalah wisata pantai dan bahari. TWP Gita Nada dengan luas terumbu karang sebesar 1279 ha memiliki nilai manfaat pariwisata Rp3.004.031.073/ha dengan jumlah total pengunjung per 1000 penduduk pada kedua zona adalah sebanyak 51.228 orang. Berdasarkan model fungsi permintaan pariwisata TWP Gita Nada pengembangan kedepan adalah wisata alam yang dikemas menjadi wisata edukasi yang fokus pada anak muda dengan minat belajar tinggi. Perbaikan aksesibiltas dan peningkatan kualitas sarana dan prasarana yang memadai akan menambah daya tarik TWP Gita Nada, dan kedepan lokasi wisata harus mampu memberikan jaminan 2H yaitu healthy dan hygiene.Title: Benefit Value of Coral Reef Ecosystem Tourism in The Marine Park Gita Nada Sekotong LombokThis study describes the use patterns of coral reef tourism in Marine Park Gita Nada. It estimates the benefit value of coral reef ecosystem with travel cost approach as a reference for planning the development of tourism areas in West Lombok Regency. The research conducted at Marine Park Gita Nada Sekotong Lombok in January to March 2020. Primary data were collected by interview questionnaires and observations of entire tourism activities in Marine Park Gita Nada. Secondary data were collected by literature review on the results of previous research and publications of related agencies. The research used zona travel cost method (ZTCM) analysis.The waters of Marine Park Gita Nada is a combination of shallow water with fringing reef circulation, and Marine Park Gita Nada is located in the border of Lombok Strait. Marine Park Gita Nada offers beach and marine attraction, and coral reefs cover 1279 ha in the area. Marine Park Gita Nada has a tourism benefit value of Rp3,004,031,073/ha with total number of visitors in both zones are 51,228 people per 1000 inhabitants. Based on tourism demand function, the future development for Marine Park Gita Nada would be educational nature-based tourism focusing on young people with high learning interests. Improvement of accessibility and quality of infrastructure will attract more tourists to TWP Gita Nada, and in the future it must guarantee the healthy and hygiene (2H) of the tourism park.

46

Coovadia, H. M. "Gita Ramjee." South African Medical Journal 110, no. 5 (April 29, 2020): 348. http://dx.doi.org/10.7196/samj.2020.v110i5.14805.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

47

&NA;. "Nifedipine GITS." Inpharma Weekly &NA;, no. 819 (January 1992): 18–19. http://dx.doi.org/10.2165/00128413-199208190-00055.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

48

Green, Andrew. "Gita Ramjee." Lancet 395, no. 10234 (May 2020): 1416. http://dx.doi.org/10.1016/s0140-6736(20)30941-7.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

49

Elliott, H. L., P. A. Meredith, DouweD Breimer, and John Urquhart. "Nifedipine GITS." Lancet 341, no. 8840 (January 1993): 306. http://dx.doi.org/10.1016/0140-6736(93)92658-g.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

50

Steinbacher, Julia, Benjamin J. Schmiedel, Antje Werner, Tina Nuebling, Corina Buechele, Ludger Grosse-Hovest, Lothar Kanz, and Helmut R. Salih. "Bimodal Induction of NK Cell Reactivity Against Acute Myeloid (AML) and Chronic Lymphoid Leukemia (CLL) by Fc-Engineered GITR-Fc Fusion Proteins." Blood 120, no. 21 (November 16, 2012): 2143. http://dx.doi.org/10.1182/blood.v120.21.2143.2143.

Повний текст джерела

Стилі APA, Harvard, Vancouver, ISO та ін.

Анотація:

Abstract Abstract 2143 NK cells play an important role in anti-tumor immunity and largely contribute to the efficacy of therapeutic strategies like allogenic stem cell transplantation in AML and application of Rituximab that induces antibody-dependent cellular cytotoxicity (ADCC) in CLL. Recently, we demonstrated that the TNF family member GITR ligand (GITRL) is expressed on leukemia cells in a high proportion of AML and CLL patients and impairs direct and Rituximab-induced reactivity of NK cells which constitutively express its counterpart GITR (e.g., Buechele et al., Leukemia 2012). Here we developed a strategy to reinforce NK anti-leukemia reactivity by combining disruption of NK-inhibitory GITR-GITRL interaction with induction of ADCC against the GITRL-expressing leukemia cells using GITR-Ig fusion proteins with modified Fc moieties. Fc parts were engineered by amino acid exchange as previously described (Lazar et al., PNAS 2006; Armour et al., Eur. J. Immunol. 1999). Compared to wild type GITR-Ig (GITR-Fc-WT), our mutants (S239D/I332E and E233P/L234V/L235A/deltaG236/A327G/A330S) displayed highly enhanced (GITR-Fc-ADCC) and abrogated (GITR-Fc-KO) affinity to the Fc(gamma)RIIIa receptor (CD16) expressed on NK cells, respectively. In functional analyses of NK cells and primary leukemia cells, GITR-Fc-KO, which does not induce ADCC, already increased NK reactivity due to disruption of GITR-GITRL interaction. Treatment with GITR-Fc-WT further enhanced NK reactivity due to modest induction of ADCC, while GITR-Fc-ADCC induced highly increased NK-mediated target cell lysis, degranulation and cytokine production in a target-antigen dependent manner. With CLL cells, combined treatment with GITR-Fc-ADCC fusion protein and Rituximab caused additive effects, resulting in significantly enhanced NK cell ADCC. Notably, the effects of our fusion proteins were observed both in an allogenic setting and when employing NK cells of patients with autologous leukemia cells as targets. Our results demonstrate that Fc-engineered GITR-Fc-ADCC fusion protein may combine both neutralization of the NK-inhibitoryeffects of GITR-GITRL interaction and targeting GITRL-expressing malignant cells for NK anti-tumor reactivity and thus constitute an attractive immunotherapeutic means for the treatment of AML and CLL. Disclosures: No relevant conflicts of interest to declare.

Статті в журналах з теми "GITC"

Оформте джерело за APA, MLA, Chicago, Harvard та іншими стилями