Artykuły w czasopismach: „Sin1”

1

McCarthy, Nicola. "An original SIN1". Nature Reviews Cancer 13, nr 12 (22.11.2013): 823. http://dx.doi.org/10.1038/nrc3641.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

2

Kruger, W., i I. Herskowitz. "A negative regulator of HO transcription, SIN1 (SPT2), is a nonspecific DNA-binding protein related to HMG1". Molecular and Cellular Biology 11, nr 8 (sierpień 1991): 4135–46. http://dx.doi.org/10.1128/mcb.11.8.4135-4146.1991.

Pełny tekst źródła

Streszczenie:

The SIN1 gene was initially identified because mutations in SIN1 bypass the need for SWI1 to activate transcription of the yeast HO gene. We show here that transcription of HO in swi1 sin1 cells efficiently utilizes the normal start site. We have cloned SIN1 and found that it is identical to the previously identified gene SPT2, mutations in which allow transcription from certain mutated regulatory regions. The predicted SIN1/SPT2 protein has a distinctive amino acid composition (45% charged residues, 25% basic and 20% acidic) and has similarity to the mammalian HMG1 protein, a nonhistone component of chromatin. We show that SIN1 is concentrated in the nucleus and binds to DNA with little or no sequence specificity in vitro. It thus exhibits properties of an HMG protein. Addition of random DNA segments to a test promoter alters regulation by SIN1 in a manner similar to addition of a segment from the HO upstream region. Functional analysis of certain SIN1 mutations suggests that SIN1 may be part of a multiprotein complex. On the basis of these results, we propose that SIN1 is a nonhistone component of chromatin which creates the proper context for transcription. Because sin1 mutants exhibit increased loss of chromosome III, SIN1 may also play a role in fidelity of chromosome segregation.

Style APA, Harvard, Vancouver, ISO itp.

3

Kruger, W., i I. Herskowitz. "A negative regulator of HO transcription, SIN1 (SPT2), is a nonspecific DNA-binding protein related to HMG1." Molecular and Cellular Biology 11, nr 8 (sierpień 1991): 4135–46. http://dx.doi.org/10.1128/mcb.11.8.4135.

Pełny tekst źródła

Streszczenie:

The SIN1 gene was initially identified because mutations in SIN1 bypass the need for SWI1 to activate transcription of the yeast HO gene. We show here that transcription of HO in swi1 sin1 cells efficiently utilizes the normal start site. We have cloned SIN1 and found that it is identical to the previously identified gene SPT2, mutations in which allow transcription from certain mutated regulatory regions. The predicted SIN1/SPT2 protein has a distinctive amino acid composition (45% charged residues, 25% basic and 20% acidic) and has similarity to the mammalian HMG1 protein, a nonhistone component of chromatin. We show that SIN1 is concentrated in the nucleus and binds to DNA with little or no sequence specificity in vitro. It thus exhibits properties of an HMG protein. Addition of random DNA segments to a test promoter alters regulation by SIN1 in a manner similar to addition of a segment from the HO upstream region. Functional analysis of certain SIN1 mutations suggests that SIN1 may be part of a multiprotein complex. On the basis of these results, we propose that SIN1 is a nonhistone component of chromatin which creates the proper context for transcription. Because sin1 mutants exhibit increased loss of chromosome III, SIN1 may also play a role in fidelity of chromosome segregation.

Style APA, Harvard, Vancouver, ISO itp.

4

Xu, Yanyan, Xue Chen i Junling Liu. "The Critical Roles of SIN1 in Platelet Activation and Myocardial Infarction". Blood 128, nr 22 (2.12.2016): 3715. http://dx.doi.org/10.1182/blood.v128.22.3715.3715.

Pełny tekst źródła

Streszczenie:

Abstract Mammalian stress-activated protein kinase interacting protein 1 (SIN1) is an essential subunit of the mTORC2 complex, which regulates Akt activation by phosphorylation of Akt at Ser473 residue. Despite the function of Akt in platelet activation and thrombosis was well studied, the role of SIN1 in platelet activation and thrombosis remains unknown. In this study, we observed that megakaryocyte/platelet specific SIN1 deficiency caused 30% reduction of platelet counts in peripheral blood probably by blockage of megakaryocyte differentiation and enhancing platelet apoptosis, suggesting that SIN1 had an important role in thrombopoiesis. More importantly, SIN1 deficiency caused a defect in platelet aggregation in response to low level of thrombin, U46619, ADP and collagen. SIN1 deficiency also exhibited diminished ability of platelet to spread on immobilized fibrinogen and the decreased rate of clot retraction in platelet-rich plasma containing SIN1 deficient platelets. mTORC2 complex analysis revealed that the expression levels of Rictor, another mTORC2 component, were significantly diminished in SIN1 deficient platelet. And SIN1 deficiency attenuated agonist-induced phosphorylation of Akt at Ser473, Thr308 and Thr450, and Gsk3β at Ser9 in platelet. SIN1 could be phosphorylated at Thr86, which correlated with the phosphorylation of Akt at Ser473 in activated platelets. Further study demonstrated that the phosphorylation levels of SIN1 at Thr86 and Akt at Ser473 and Thr450, but not at Thr308 were enhanced in the platelets collected from ST-segment elevation myocardial infarction (STEMI) patients, indicating that SIN1 activation correlated with myocardial infarction process. A mouse model of chronic myocardial infarction (MI) was performed and the results demonstrated that platelet-specific SIN1 deficient mice had less platelet activation, reduced MI size, and improved post-MI heart function. In conclusion, SIN1 plays critical roles in platelet activation, MI and post-MI heart failure, therefore serves as a target for therapeutic intervention in the thrombosis and myocardial infarction. Disclosures No relevant conflicts of interest to declare.

Style APA, Harvard, Vancouver, ISO itp.

5

Ray, A., J. D. Lang, T. Golden i S. Ray. "SHORT INTEGUMENT (SIN1), a gene required for ovule development in Arabidopsis, also controls flowering time". Development 122, nr 9 (1.09.1996): 2631–38. http://dx.doi.org/10.1242/dev.122.9.2631.

Pełny tekst źródła

Streszczenie:

The short integument (sin1) mutation causes a female-specific infertility, and a defect in the control of time to flowering in Arabidopsis. Female sterility of Sin- plants is due to abnormal ovule integument development and aberrant differentiation of the megagametophyte in a subset of ovules. An additional defect of sin1 mutants is the production of an increased number of vegetative leaf and inflorescence primordia leading to delayed flowering. The delayed flowering phenotype of sin1-1 is not due to a defect in the perception of day length periodicity or in gibberellic acid metabolism. Phenotypes of double mutant combinations of sin1 with terminalflower (tfl1) indicate that SIN1 activity is required for precocious floral induction typical in a tfl1 mutant. Unexpectedly, sin1-1 tfl1-1 plants do not make pollen, thus revealing a novel role for TFL1 in the anther. Early flowers of sin1-1 ap1-1 double mutants are transformed to long inflorescence-like shoots. A genetic model for the role of SIN1 in flowering time control is proposed.

Style APA, Harvard, Vancouver, ISO itp.

6

Zhou, Yang. "Exploring the emergence of the postverbal sin1 先 in Cantonese". Language and Linguistics / 語言暨語言學 19, nr 2 (15.03.2018): 333–75. http://dx.doi.org/10.1075/lali.00012.zho.

Pełny tekst źródła

Streszczenie:

Abstract Sin1 先 as a function word in contemporary Cantonese encodes a number of grammatical and pragmatic meanings. As its most prominent feature in syntax, it predominantly occurs in the postverbal position while indicating the meaning of ‘first’. This paper explores the emergence of the postverbal sin1 先 ‘first’ in Cantonese. We first examine the word order typology on the element for ‘first’ in the languages and dialects of southern coastal China. In this linguistic area, the postverbal elements for ‘first’ in Chinese dialects are contact-induced by Tai-Kadai and Hmong-Mien languages; whereas sin1 先 ‘first’ in the mainstream Cantonese shows a stronger tendency to be placed in the postverbal position than its counterparts in other Chinese dialects. We then discuss the word order and semantic changes of sin1 先 from 1820s to 1960s based on Cantonese historical materials. Besides the pressure of language contact, the formation of the postverbal sin1 先 ‘first’ has been further triggered by the semantic motivation to formally differentiate the ‘precedent-subsequent’ polysemy within sin1 先 itself. In short, the emergence of the postverbal sin1 先 ‘first’ in Cantonese has been a two-stage process, dually driven by external and internal causes, respectively.

Style APA, Harvard, Vancouver, ISO itp.

7

Cameron, Angus J. M., Mark D. Linch, Adrian T. Saurin, Cristina Escribano i Peter J. Parker. "mTORC2 targets AGC kinases through Sin1-dependent recruitment". Biochemical Journal 439, nr 2 (28.09.2011): 287–97. http://dx.doi.org/10.1042/bj20110678.

Pełny tekst źródła

Streszczenie:

The protein kinase TOR (target of rapamycin) is a key regulator of cell growth and metabolism with significant clinical relevance. In mammals, TOR signals through two distinct multi-protein complexes, mTORC1 and mTORC2 (mammalian TOR complex 1 and 2 respectively), the subunits of which appear to define the operational pathways. Rapamycin selectively targets mTORC1 function, and the emergence of specific ATP-competitive kinase inhibitors has enabled assessment of dual mTORC1 and mTORC2 blockade. Little is known, however, of the molecular action of mTORC2 components or the relative importance of targeting this pathway. In the present study, we have identified the mTORC2 subunit Sin1 as a direct binding partner of the PKC (protein kinase C) ϵ kinase domain and map the interaction to the central highly conserved region of Sin1. Exploiting the conformational dependence for PKC phosphorylation, we demonstrate that mTORC2 is essential for acute priming of PKC. Inducible expression of Sin1 mutants, lacking the PKC-interaction domain, displaces endogenous Sin1 from mTORC2 and disrupts PKC phosphorylation. PKB (protein kinase B)/Akt phosphorylation is also suppressed by these Sin1 mutants, but not the mTORC1 substrate p70S6K (S6 kinase), providing evidence that Sin1 serves as a selectivity adaptor for the recruitment of mTORC2 targets. This inducible selective mTORC2 intervention is used to demonstrate a key role for mTORC2 in cell proliferation in three-dimensional culture.

Style APA, Harvard, Vancouver, ISO itp.

8

Castel, Pau, Srisathiyanarayanan Dharmaiah, Matthew J. Sale, Simon Messing, Gabrielle Rizzuto, Antonio Cuevas-Navarro, Alice Cheng i in. "RAS interaction with Sin1 is dispensable for mTORC2 assembly and activity". Proceedings of the National Academy of Sciences 118, nr 33 (11.08.2021): e2103261118. http://dx.doi.org/10.1073/pnas.2103261118.

Pełny tekst źródła

Streszczenie:

RAS proteins are molecular switches that interact with effector proteins when bound to guanosine triphosphate, stimulating downstream signaling in response to multiple stimuli. Although several canonical downstream effectors have been extensively studied and tested as potential targets for RAS-driven cancers, many of these remain poorly characterized. In this study, we undertook a biochemical and structural approach to further study the role of Sin1 as a RAS effector. Sin1 interacted predominantly with KRAS isoform 4A in cells through an atypical RAS-binding domain that we have characterized by X-ray crystallography. Despite the essential role of Sin1 in the assembly and activity of mTORC2, we find that the interaction with RAS is not required for these functions. Cells and mice expressing a mutant of Sin1 that is unable to bind RAS are proficient for activation and assembly of mTORC2. Our results suggest that Sin1 is a bona fide RAS effector that regulates downstream signaling in an mTORC2-independent manner.

Style APA, Harvard, Vancouver, ISO itp.

9

Pérez-Martín, José, i Alexander D. Johnson. "The C-Terminal Domain of Sin1 Interacts with the SWI-SNF Complex in Yeast". Molecular and Cellular Biology 18, nr 7 (1.07.1998): 4157–64. http://dx.doi.org/10.1128/mcb.18.7.4157.

Pełny tekst źródła

Streszczenie:

ABSTRACT In the yeast Saccharomyces cerevisiae, the SWI-SNF complex has been proposed to antagonize the repressive effects of chromatin by disrupting nucleosomes. The SIN genes were identified as suppressors of defects in the SWI-SNF complex, and theSIN1 gene encodes an HMG1-like protein that has been proposed to be a component of chromatin. Specific mutations (sin mutations) in both histone H3 and H4 genes produce the same phenotypic effects as do mutations in the SIN1 gene. In this study, we demonstrate that Sin1 and the H3 and H4 histones interact genetically and that the C terminus of Sin1 physically associates with components of the SWI-SNF complex. In addition, we demonstrate that this interaction is blocked in the full-length Sin1 protein by the N-terminal half of the protein. Based on these and additional results, we propose that Sin1 acts as a regulatable bridge between the SWI-SNF complex and the nucleosome.

Style APA, Harvard, Vancouver, ISO itp.

10

Zdetsis, Aristides D. "Fluxional and aromatic behavior in small magic silicon clusters: A full ab initio study of Sin, Sin1−, Sin2−, and Sin1+, n=6, 10 clusters". Journal of Chemical Physics 127, nr 1 (7.07.2007): 014314. http://dx.doi.org/10.1063/1.2746030.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

11

Yuan, Yuanyang, Bangfen Pan, Haipeng Sun, Guoqiang Chen, Bing Su i Ying Huang. "Characterization of Sin1 Isoforms Reveals an mTOR-Dependent and Independent Function of Sin1γ". PLOS ONE 10, nr 8 (11.08.2015): e0135017. http://dx.doi.org/10.1371/journal.pone.0135017.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

12

Ouyang, Xinxing, Yuheng Han, Guojun Qu, Man Li, Ningbo Wu, Hongzhi Liu, Omotooke Arojo i in. "Metabolic regulation of T cell development by Sin1–mTORC2 is mediated by pyruvate kinase M2". Journal of Molecular Cell Biology 11, nr 2 (14.11.2018): 93–106. http://dx.doi.org/10.1093/jmcb/mjy065.

Pełny tekst źródła

Streszczenie:

Abstract Glucose metabolism plays a key role in thymocyte development. The mammalian target of rapamycin complex 2 (mTORC2) is a critical regulator of cell growth and metabolism, but its role in early thymocyte development and metabolism has not been fully studied. We show here that genetic ablation of Sin1, an essential component of mTORC2, in T lineage cells results in severely impaired thymocyte development at the CD4−CD8− double negative (DN) stages but not at the CD4+CD8+ double positive (DP) or later stages. Notably, Sin1-deficient DN thymocytes show markedly reduced proliferation and glycolysis. Importantly, we discover that the M2 isoform of pyruvate kinase (PKM2) is a novel and crucial Sin1 effector in promoting DN thymocyte development and metabolism. At the molecular level, we show that Sin1–mTORC2 controls PKM2 expression through an AKT-dependent PPAR-γ nuclear translocation. Together, our study unravels a novel mTORC2−PPAR-γ−PKM2 pathway in immune-metabolic regulation of early thymocyte development.

Style APA, Harvard, Vancouver, ISO itp.

13

Ruan, Chun, Xinxing Ouyang, Hongzhi Liu, Song Li, Jingsi Jin, Weiyi Tang, Yu Xia i Bing Su. "Sin1-mediated mTOR signaling in cell growth, metabolism and immune response". National Science Review 6, nr 6 (1.11.2019): 1149–62. http://dx.doi.org/10.1093/nsr/nwz171.

Pełny tekst źródła

Streszczenie:

Abstract The mammalian target of rapamycin (mTOR) is an evolutionarily conserved Ser/Thr protein kinase with essential cellular function via processing various extracellular and intracellular inputs. Two distinct multi-protein mTOR complexes (mTORC), mTORC1 and mTORC2, have been identified and well characterized in eukaryotic cells from yeast to human. Sin1, which stands for Sty1/Spc1-interacting protein1, also known as mitogen-activated protein kinase (MAPK) associated protein (MAPKAP)1, is an evolutionarily conserved adaptor protein. Mammalian Sin1 interacts with many cellular proteins, but it has been widely studied as an essential component of mTORC2, and it is crucial not only for the assembly of mTORC2 but also for the regulation of its substrate specificity. In this review, we summarize our current knowledge of the structure and functions of Sin1, focusing specifically on its protein interaction network and its roles in the mTOR pathway that could account for various cellular functions of mTOR in growth, metabolism, immunity and cancer.

Style APA, Harvard, Vancouver, ISO itp.

14

Zohar, Keren, Elyad Lezmi, Tsiona Eliyahu i Michal Linial. "Ladostigil Attenuates Induced Oxidative Stress in Human Neuroblast-like SH-SY5Y Cells". Biomedicines 9, nr 9 (17.09.2021): 1251. http://dx.doi.org/10.3390/biomedicines9091251.

Pełny tekst źródła

Streszczenie:

A hallmark of the aging brain is the robust inflammation mediated by microglial activation. Pathophysiology of common neurodegenerative diseases involves oxidative stress and neuroinflammation. Chronic treatment of aging rats by ladostigil, a compound with antioxidant and anti-inflammatory function, prevented microglial activation and learning deficits. In this study, we further investigate the effect of ladostigil on undifferentiated SH-SY5Y cells. We show that SH-SY5Y cells exposed to acute (by H2O2) or chronic oxidative stress (by Sin1, 3-morpholinosydnonimine) induced apoptotic cell death. However, in the presence of ladostigil, the decline in cell viability and the increase of oxidative levels were partially reversed. RNA-seq analysis showed that prolonged oxidation by Sin1 resulted in a simultaneous reduction of the expression level of endoplasmic reticulum (ER) genes that participate in proteostasis. By comparing the differential gene expression profile of Sin1 treated cells to cells incubated with ladostigil before being exposed to Sin1, we observed an over-expression of Clk1 (Cdc2-like kinase 1) which was implicated in psychophysiological stress in mice and Alzheimer’s disease. Ladostigil also suppressed the expression of Ccpg1 (Cell cycle progression 1) and Synj1 (Synaptojanin 1) that are involved in ER-autophagy and endocytic pathways. We postulate that ladostigil alleviated cell damage induced by oxidation. Therefore, under conditions of chronic stress that are observed in the aging brain, ladostigil may block oxidative stress processes and consequently reduce neurotoxicity.

Style APA, Harvard, Vancouver, ISO itp.

15

Chi, Hongbo. "Sin1–mTORC2 signaling drives glycolysis of developing thymocytes". Journal of Molecular Cell Biology 11, nr 2 (29.11.2018): 91–92. http://dx.doi.org/10.1093/jmcb/mjy078.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

16

Yuan, Hai-Xin, i Kun-Liang Guan. "The SIN1-PH Domain Connects mTORC2 to PI3K". Cancer Discovery 5, nr 11 (listopad 2015): 1127–29. http://dx.doi.org/10.1158/2159-8290.cd-15-1125.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

17

Xu, Hui, Tong Cao, Xiaoqing Zhang, Ying Shi, Qing Zhang, Shuo Chai, Li Yu i in. "Nitidine Chloride Inhibits SIN1 Expression in Osteosarcoma Cells". Molecular Therapy - Oncolytics 12 (marzec 2019): 224–34. http://dx.doi.org/10.1016/j.omto.2019.01.005.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

18

Pollard, K. J., i C. L. Peterson. "Role for ADA/GCN5 products in antagonizing chromatin-mediated transcriptional repression." Molecular and Cellular Biology 17, nr 11 (listopad 1997): 6212–22. http://dx.doi.org/10.1128/mcb.17.11.6212.

Pełny tekst źródła

Streszczenie:

The Saccharomyces cerevisiae SWI/SNF complex is a 2-MDa multimeric assembly that facilitates transcriptional enhancement by antagonizing chromatin-mediated transcriptional repression. We show here that mutations in ADA2, ADA3, and GCN5, which are believed to encode subunits of a nuclear histone acetyltransferase complex, cause phenotypes strikingly similar to that of swi/snf mutants. ADA2, ADA3, and GCN5 are required for full expression of all SWI/SNF-dependent genes tested, including HO, SUC2, INO1, and Ty elements. Furthermore, mutations in the SIN1 gene, which encodes a nonhistone chromatin component, or mutations in histone H3 or H4 partially alleviate the transcriptional defects caused by ada/gcn5 or swi/snf mutations. We also find that ada2 swi1, ada3 swi1, and gcn5 swi1 double mutants are inviable and that mutations in SIN1 allow viability of these double mutants. We have partially purified three chromatographically distinct GCN5-dependent acetyltransferase activities, and we show that these enzymes can acetylate both histones and Sin1p. We propose a model in which the ADA/GCN5 and SWI/SNF complexes facilitate activator function by acting in concert to disrupt or modify chromatin structure.

Style APA, Harvard, Vancouver, ISO itp.

19

Kolenko, Yulia G., Iryna A. Volovyk, Natalia V. Bidenko, Konstantin O. Mialkivskyi i Iryna M. Tkachenko. "BUCCAL CELL MICRONUCLEI AMONG PATIENTS WITH ORAL LEUKOPLAKIA". Wiadomości Lekarskie 75, nr 7 (2022): 1713–17. http://dx.doi.org/10.36740/wlek202207119.

Pełny tekst źródła

Streszczenie:

The aim: The purpose of research was to evaluate the efficiency of micronucleus test in buccal cells for the diagnosis of oral leukoplakia. Materials and methods: We have conducted a comprehensive clinical and laboratory examination of 155 patients with oral leukoplakia. It was conducted histological examination leukoplakia mucosal sites, to assess the buccal epithelium cell micronucleus test was carried out. Results: Histological evaluation of the material was made according to the classification of leukoplakia WHO (2005). They are established 10 (14%) sites unmodified mucosa, 10 (14%) of the samples hyperkeratosis without atypia, 14 (19%) biopsies hyperkeratosis SIN1, 15 (21%) of hyperkeratosis SIN2, 10 (14%) -- SIN3 and 13 (18 %) of the cases of squamous cell carcinoma. Micronuclei, whose appearance is caused by violation of differentiation of epithelial cells, were found in patients with leukoplakia, the detection of micronuclei almost equally high as in patients with leukoplakia SIN2, and with SIN3 (a difference of 1.3 times (p <0,05, rxy = + 0.271)), and consequently the probability of occurrence of tumoral diseases of the oral mucosa or malignancy existing large. Conclusions: Thus, on the background of the general increase in proliferative activity of epithelial cells with increasing SIN, for each treatment group revealed the appearance of micronuclei in buccal cells. And the frequency of micronuclei and the fourth type of increases with hyperplasia, indicating an increase in the likelihood of malignancy and cancer of the oral mucosa in patients with leukoplakia SIN3.

Style APA, Harvard, Vancouver, ISO itp.

20

Kitamura, Nao, Nobuyuki Fujiwara, Koji Hayakawa, Takashi Ohama i Koichi Sato. "Protein phosphatase 6 promotes neurite outgrowth by dephosphorylating SIN1". Proceedings for Annual Meeting of The Japanese Pharmacological Society 95 (2022): 1—SS—51. http://dx.doi.org/10.1254/jpssuppl.95.0_1-ss-51.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

21

Zohar, Keren, Eliran Giladi, Tsiona Eliyahu i Michal Linial. "Oxidative Stress and Its Modulation by Ladostigil Alter the Expression of Abundant Long Non-Coding RNAs in SH-SY5Y Cells". Non-Coding RNA 8, nr 6 (25.10.2022): 72. http://dx.doi.org/10.3390/ncrna8060072.

Pełny tekst źródła

Streszczenie:

Neurodegenerative disorders, brain injury, and the decline in cognitive function with aging are accompanied by a reduced capacity of cells in the brain to cope with oxidative stress and inflammation. In this study, we focused on the response to oxidative stress in SH-SY5Y, a human neuroblastoma cell line. We monitored the viability of the cells in the presence of oxidative stress. Such stress was induced by hydrogen peroxide or by Sin1 (3-morpholinosydnonimine) that generates reactive oxygen and nitrogen species (ROS and RNS). Both stressors caused significant cell death. Our results from the RNA-seq experiments show that SH-SY5Y cells treated with Sin1 for 24 h resulted in 94 differently expressed long non-coding RNAs (lncRNAs), including many abundant ones. Among the abundant lncRNAs that were upregulated by exposing the cells to Sin1 were those implicated in redox homeostasis, energy metabolism, and neurodegenerative diseases (e.g., MALAT1, MIAT, GABPB1-AS1, NEAT1, MIAT, GABPB1-AS1, and HAND2-AS1). Another group of abundant lncRNAs that were significantly altered under oxidative stress included cancer-related SNHG family members. We tested the impact of ladostigil, a bifunctional reagent with antioxidant and anti-inflammatory properties, on the lncRNA expression levels. Ladostigil was previously shown to enhance learning and memory in the brains of elderly rats. In SH-SY5Y cells, several lncRNAs involved in transcription regulation and the chromatin structure were significantly induced by ladostigil. We anticipate that these poorly studied lncRNAs may act as enhancers (eRNA), regulating transcription and splicing, and in competition for miRNA binding (ceRNA). We found that the induction of abundant lncRNAs, such as MALAT1, NEAT-1, MIAT, and SHNG12, by the Sin1 oxidative stress paradigm specifies only the undifferentiated cell state. We conclude that a global alteration in the lncRNA profiles upon stress in SH-SY5Y may shift cell homeostasis and is an attractive in vitro system to characterize drugs that impact the redox state of the cells and their viability.

Style APA, Harvard, Vancouver, ISO itp.

22

Wilkinson, M. G. "Sin1: an evolutionarily conserved component of the eukaryotic SAPK pathway". EMBO Journal 18, nr 15 (2.08.1999): 4210–21. http://dx.doi.org/10.1093/emboj/18.15.4210.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

23

Shpungin, S., A. Liberzon, H. Bangio, E. Yona i D. J. Katcoff. "Association of yeast SIN1 with the tetratrico peptide repeats of CDC23." Proceedings of the National Academy of Sciences 93, nr 16 (6.08.1996): 8274–77. http://dx.doi.org/10.1073/pnas.93.16.8274.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

24

Yang, Guang, Danielle S. Murashige, Sean J. Humphrey i David E. James. "A Positive Feedback Loop between Akt and mTORC2 via SIN1 Phosphorylation". Cell Reports 12, nr 6 (sierpień 2015): 937–43. http://dx.doi.org/10.1016/j.celrep.2015.07.016.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

25

Lefebvre, L., i M. Smith. "Mutational and functional analysis of dominant SPT2 (SIN1) suppressor alleles in Saccharomyces cerevisiae". Molecular and Cellular Biology 13, nr 9 (wrzesień 1993): 5393–407. http://dx.doi.org/10.1128/mcb.13.9.5393-5407.1993.

Pełny tekst źródła

Streszczenie:

The Saccharomyces cerevisiae SPT2 gene was identified by genetic screens for mutations which are suppressors of Ty and delta insertional mutations at the HIS4 locus. The ability of spt2 mutations to suppress the transcriptional interference caused by the delta promoter insertion his-4-912 delta correlates with an increase in wild-type HIS4 mRNA levels. The SPT2 gene is identical to SIN1, which codes for a factor genetically defined as a negative regulator of HO transcription. Mutations in SPT2/SIN1 suppress the effects of trans-acting mutations in SWI genes and of partial deletions in the C-terminal domain of the largest subunit of RNA polymerase II. Nuclear localization and protein sequence similarities suggested that the SPT2/SIN1 protein may be related to the nonhistone chromosomal protein HMG1. To assess the significance of this structural similarity and identify domains of SPT2 functionally important in the regulation of his4-912 delta, we have studied recessive and dominant spt2 mutations created by in vitro mutagenesis. We show here that several alleles carrying C-terminal deletions as well as point mutations in the C-terminal domain of the SPT2 protein exhibit a dominant suppressor phenotype. C-terminal basic residues necessary for wild-type SPT2 protein function which are absent from HMG1 have been identified. The competence of these mutant SPT2 proteins to interfere with the maintenance of the His- (Spt+) phenotype of a his4-912 delta SPT2+ strain is lost by deletion of internal HMG1-like sequences and is sensitive to the wild-type SPT2+ gene dosage. Using cross-reacting antipeptide polyclonal antibodies, we demonstrate that the intracellular level of the wild-type SPT2 protein is not affected in presence of dominant mutations and furthermore that the reversion of the dominance by internal deletion of HMG1-like sequences is not mediated by altered production or stability of the mutant polypeptides. Our results suggest that the products of dominant alleles directly compete with the wild-type protein. On the basis of primary sequence similarities, we propose that an HMG-box-like motif is required for SPT2 function in vivo and that this motif also is necessary for the dominant suppressor phenotype exhibited by some mutant SPT2 alleles.

Style APA, Harvard, Vancouver, ISO itp.

26

Lefebvre, L., i M. Smith. "Mutational and functional analysis of dominant SPT2 (SIN1) suppressor alleles in Saccharomyces cerevisiae." Molecular and Cellular Biology 13, nr 9 (wrzesień 1993): 5393–407. http://dx.doi.org/10.1128/mcb.13.9.5393.

Pełny tekst źródła

Streszczenie:

The Saccharomyces cerevisiae SPT2 gene was identified by genetic screens for mutations which are suppressors of Ty and delta insertional mutations at the HIS4 locus. The ability of spt2 mutations to suppress the transcriptional interference caused by the delta promoter insertion his-4-912 delta correlates with an increase in wild-type HIS4 mRNA levels. The SPT2 gene is identical to SIN1, which codes for a factor genetically defined as a negative regulator of HO transcription. Mutations in SPT2/SIN1 suppress the effects of trans-acting mutations in SWI genes and of partial deletions in the C-terminal domain of the largest subunit of RNA polymerase II. Nuclear localization and protein sequence similarities suggested that the SPT2/SIN1 protein may be related to the nonhistone chromosomal protein HMG1. To assess the significance of this structural similarity and identify domains of SPT2 functionally important in the regulation of his4-912 delta, we have studied recessive and dominant spt2 mutations created by in vitro mutagenesis. We show here that several alleles carrying C-terminal deletions as well as point mutations in the C-terminal domain of the SPT2 protein exhibit a dominant suppressor phenotype. C-terminal basic residues necessary for wild-type SPT2 protein function which are absent from HMG1 have been identified. The competence of these mutant SPT2 proteins to interfere with the maintenance of the His- (Spt+) phenotype of a his4-912 delta SPT2+ strain is lost by deletion of internal HMG1-like sequences and is sensitive to the wild-type SPT2+ gene dosage. Using cross-reacting antipeptide polyclonal antibodies, we demonstrate that the intracellular level of the wild-type SPT2 protein is not affected in presence of dominant mutations and furthermore that the reversion of the dominance by internal deletion of HMG1-like sequences is not mediated by altered production or stability of the mutant polypeptides. Our results suggest that the products of dominant alleles directly compete with the wild-type protein. On the basis of primary sequence similarities, we propose that an HMG-box-like motif is required for SPT2 function in vivo and that this motif also is necessary for the dominant suppressor phenotype exhibited by some mutant SPT2 alleles.

Style APA, Harvard, Vancouver, ISO itp.

27

Chen, Chien-Hung, Vladimir Kiyan, Assylbek A. Zhylkibayev, Dubek Kazyken, Olga Bulgakova, Kent E. Page, Rakhmet I. Bersimbaev, Eric Spooner i Dos D. Sarbassov. "Autoregulation of the Mechanistic Target of Rapamycin (mTOR) Complex 2 Integrity Is Controlled by an ATP-dependent Mechanism". Journal of Biological Chemistry 288, nr 38 (8.08.2013): 27019–30. http://dx.doi.org/10.1074/jbc.m113.498055.

Pełny tekst źródła

Streszczenie:

Nutrients are essential for living organisms because they fuel biological processes in cells. Cells monitor nutrient abundance and coordinate a ratio of anabolic and catabolic reactions. Mechanistic target of rapamycin (mTOR) signaling is the essential nutrient-sensing pathway that controls anabolic processes in cells. The central component of this pathway is mTOR, a highly conserved and essential protein kinase that exists in two distinct functional complexes. The nutrient-sensitive mTOR complex 1 (mTORC1) controls cell growth and cell size by phosphorylation of the regulators of protein synthesis S6K1 and 4EBP1, whereas its second complex, mTORC2, regulates cell proliferation by functioning as the regulatory kinase of Akt and other members of the AGC kinase family. The regulation of mTORC2 remains poorly characterized. Our study shows that the cellular ATP balance controls a basal kinase activity of mTORC2 that maintains the integrity of mTORC2 and phosphorylation of Akt on the turn motif Thr-450 site. We found that mTOR stabilizes SIN1 by phosphorylation of its hydrophobic and conserved Ser-260 site to maintain the integrity of mTORC2. The optimal kinase activity of mTORC2 requires a concentration of ATP above 1.2 mm and makes this kinase complex highly sensitive to ATP depletion. We found that not amino acid but glucose deprivation of cells or acute ATP depletion prevented the mTOR-dependent phosphorylation of SIN1 on Ser-260 and Akt on Thr-450. In a low glucose medium, the cells carrying a substitution of SIN1 with its phosphomimetic mutant show an increased rate of cell proliferation related to a higher abundance of mTORC2 and phosphorylation of Akt. Thus, the homeostatic ATP sensor mTOR controls the integrity of mTORC2 and phosphorylation of Akt on the turn motif site.

Style APA, Harvard, Vancouver, ISO itp.

28

Dumortier, Julien G., i Nicolas B. David. "The TORC2 Component, Sin1, Controls Migration of Anterior Mesendoderm during Zebrafish Gastrulation". PLOS ONE 10, nr 2 (24.02.2015): e0118474. http://dx.doi.org/10.1371/journal.pone.0118474.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

29

Wang, Jian-Qiu, Jian-Hong Chen, Yen-Chung Chen, Mei-Yu Chen, Chia-Ying Hsieh, Shu-Chun Teng i Kou-Juey Wu. "Interaction between NBS1 and the mTOR/Rictor/SIN1 Complex through Specific Domains". PLoS ONE 8, nr 6 (6.06.2013): e65586. http://dx.doi.org/10.1371/journal.pone.0065586.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

30

Schroder, Wayne, Nicole Cloonan, Gillian Bushell i Tom Sculley. "Alternative polyadenylation and splicing of mRNAs transcribed from the human Sin1 gene". Gene 339 (wrzesień 2004): 17–23. http://dx.doi.org/10.1016/j.gene.2004.07.001.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

31

Yingying, Xiang, Wang Caijuan, Yue Yenan, Tang Yuqin, Cai Xueqin i Wu Zhongming. "The Effect of SIN1 and Microtubules on Insulin Induced PKC ζ Activation". Medical Science Monitor 23 (28.07.2017): 3666–72. http://dx.doi.org/10.12659/msm.905555.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

32

Wang, Q., J. Zhu, Y.-W. Wang, Y. Dai, Y.-L. Wang, C. Wang, J. Liu, A. Baker, N. H. Colburn i H.-S. Yang. "Tumor suppressor Pdcd4 attenuates Sin1 translation to inhibit invasion in colon carcinoma". Oncogene 36, nr 45 (10.07.2017): 6225–34. http://dx.doi.org/10.1038/onc.2017.228.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

33

Okuhashi, Yuki, Mai Itoh, Nobuo Nara i Shuji Tohda. "Effects of NOTCH Knockdown on the Proliferation and mTOR Signaling of T-ALL and AML Cell Lines". Blood 122, nr 21 (15.11.2013): 1396. http://dx.doi.org/10.1182/blood.v122.21.1396.1396.

Pełny tekst źródła

Streszczenie:

Abstract Background The activation of Notch is crucial for the growth of T-ALL cells with NOTCH1 mutations. The precise roles of Notch signaling in AML cells are not fully understood, although the growth of AML cells is diversely affected by Notch ligand stimulation as we previously reported. We also reported the effects of γ-secretase inhibitors (GSIs), which block Notch activation, on the growth of leukemia cells. However, these effects might not necessarily be due to Notch inhibition as GSIs also exhibit some off-target effects. To elucidate the roles of Notch signaling in leukemia cells, we examined the effects of small interfering RNA (siRNA)-mediated knockdown of NOTCH1 and NOTCH2on cell proliferation and down-stream signaling pathways such as mTOR signaling in T-ALL and AML cell lines. Methods Two T-ALL cell lines (DND-41 and KOPT-K1) and 2 AML cell lines (THP-1 and TMD7) were used in this study. The cells were transfected with siRNAs targeting NOTCH1 (siN1), NOTCH2 (siN2), or control siRNA by using the pipette tip chamber-based electroporation system. The effects of siN1 and siN2 transfection on cell proliferation and induction of apoptosis were examined using a colorimetric WST-8 assay and by observing cytospin preparations of the harvested cells, respectively. The effects of the siRNA-transfection on the mRNA and protein expression were examined by quantitative RT-PCR and immunoblotting, respectively. Results Transfection with siN1 and siN2 selectively suppressed the expression of Notch1 and Notch2 mRNA and protein, respectively. In T-ALL cell lines, NOTCH1 knockdown as well as NOTCH2 knockdown suppressed cell proliferation and induced apoptosis. Immunoblot analysis showed that Myc expression was downregulated in NOTCH1-knockdown cells but not affected in NOTCH2-knockdown cells. In AML cell lines, cell proliferation was not significantly affected by NOTCH siRNAs. NOTCH2 knockdown increased the level of cleaved Notch1 fragment without increasing Notch1 expression. The knockdown of NOTCH1 and NOTCH2 reduced the expression and phosphorylation of mTOR protein in THP-1 cells. To confirm this finding, we examined the effects of activation of Notch by the recombinant Notch ligands, Jagged1 and Delta1, on the expression of mTOR protein. The activation of Notch resulted in an increase in the level of the mTOR protein and its phosphorylation in THP-1 cells. Thus, siRNA-transfection and ligand stimulation of Notch showed contrasting effects. Phosphorylation of Akt, 4E-BP1, and S6K was also induced after the stimulation. Discussion Using siRNA-mediated knockdown experiments, we found that Notch2 signaling plays a role in the growth of T-ALL cells, independent of Myc expression. The autonomous activation of Notch signaling in AML cells had little effect on the proliferation of these cells. Notch2 protein seemed to be involved in the activation of Notch1 in AML cells. Regarding the crosstalk between Notch and mTOR signaling, it is known that the Notch-induced Hes1 protein suppresses PTEN transcription, resulting in the promotion of Akt phosphorylation. We found an alternative pathway linking Notch and mTOR signaling in THP-1 cells in which the PTEN gene is homozygously deleted. In THP-1 cells, Notch activation promotes the expression and phosphorylation of the mTOR protein and the activation of mTOR signaling. These findings would contribute to the development of effective Notch-targeted therapy against leukemia. Disclosures: No relevant conflicts of interest to declare.

Style APA, Harvard, Vancouver, ISO itp.

34

Baxter, Bonnie K., i Elizabeth A. Craig. "Suppression of an Hsp70 Mutant Phenotype in Saccharomyces cerevisiae through Loss of Function of the Chromatin Component Sin1p/Spt2p". Journal of Bacteriology 180, nr 24 (15.12.1998): 6484–92. http://dx.doi.org/10.1128/jb.180.24.6484-6492.1998.

Pełny tekst źródła

Streszczenie:

ABSTRACT The Ssa subfamily of Hsp70 molecular chaperones in the budding yeast Saccharomyces cerevisiae has four members, encoded bySSA1, SSA2, SSA3, andSSA4. Deletion of the two constitutively expressed genes,SSA1 and SSA2, results in cells which are slow growing and temperature sensitive. In this study, we demonstrate that an extragenic suppressor of the temperature sensitivity of ssa1 ssa2 strains, EXA1-1, is a loss-of-function mutation in SIN1/SPT2, which encodes a nonhistone component of chromatin. Loss of function of Sin1p leads to overexpression ofSSA3 in the ssa1 ssa2 mutant background, at a level which is sufficient to mediate suppression. In a strain which is wild type for SSA genes, we detected no effect of Sin1p on Ssa3p expression except under conditions of heat shock. Existing data indicate that expression of SSA3 in thessa1 ssa2 mutant background as well as in heat-shocked wild-type strains is mediated by the heat shock transcription factor HSF. Our findings suggest that it is HSF-mediated induction of SSA3 which is modulated by Sin1p. TheEXA1-1 suppressor mutation thus improves the growth ofssa1 ssa2 strains by selectively increasing HSF-mediated expression of SSA3.

Style APA, Harvard, Vancouver, ISO itp.

35

Li, Man, Adam S. Lazorchak, Xinxing Ouyang, Huihui Zhang, Hongzhi Liu, Omotooke A. Arojo, Lichong Yan i in. "Sin1/mTORC2 regulate B cell growth and metabolism by activating mTORC1 and Myc". Cellular & Molecular Immunology 16, nr 9 (31.01.2019): 757–69. http://dx.doi.org/10.1038/s41423-018-0185-x.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

36

Katcoff, Don J., Eyal Yona, Gitit Hershkovits, Hadas Friedman, Yael Cohen i Orly Dgany. "SIN1 interacts with a protein that binds the URS1 region of the yeastHOgene". Nucleic Acids Research 21, nr 22 (1993): 5101–9. http://dx.doi.org/10.1093/nar/21.22.5101.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

37

Lazorchak, Adam S., Dou Liu, Valeria Facchinetti, Annarita Di Lorenzo, William C. Sessa, David G. Schatz i Bing Su. "Sin1-mTORC2 Suppresses rag and il7r Gene Expression through Akt2 in B Cells". Molecular Cell 39, nr 3 (sierpień 2010): 433–43. http://dx.doi.org/10.1016/j.molcel.2010.07.031.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

38

Schroder, Wayne A., Marion Buck, Nicole Cloonan, John F. Hancock, Andreas Suhrbier, Tom Sculley i Gillian Bushell. "Human Sin1 contains Ras-binding and pleckstrin homology domains and suppresses Ras signalling". Cellular Signalling 19, nr 6 (czerwiec 2007): 1279–89. http://dx.doi.org/10.1016/j.cellsig.2007.01.013.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

39

Xu, Jiangfeng, Xuedong Li, Hao Yang, RuiMin Chang, Chenchen Kong i Lianyue Yang. "SIN1 promotes invasion and metastasis of hepatocellular carcinoma by facilitating epithelial-mesenchymal transition". Cancer 119, nr 12 (5.04.2013): 2247–57. http://dx.doi.org/10.1002/cncr.28023.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

40

Pearce, Laura R., Xu Huang, Jérôme Boudeau, Rafał Pawłowski, Stephan Wullschleger, Maria Deak, Adel F. M. Ibrahim, Robert Gourlay, Mark A. Magnuson i Dario R. Alessi. "Identification of Protor as a novel Rictor-binding component of mTOR complex-2". Biochemical Journal 405, nr 3 (13.07.2007): 513–22. http://dx.doi.org/10.1042/bj20070540.

Pełny tekst źródła

Streszczenie:

The mTOR (mammalian target of rapamycin) protein kinase is an important regulator of cell growth. Two complexes of mTOR have been identified: complex 1, consisting of mTOR–Raptor (regulatory associated protein of mTOR)–mLST8 (termed mTORC1), and complex 2, comprising mTOR–Rictor (rapamycininsensitive companion of mTOR)–mLST8–Sin1 (termed mTORC2). mTORC1 phosphorylates the p70 ribosomal S6K (S6 kinase) at its hydrophobic motif (Thr389), whereas mTORC2 phosphorylates PKB (protein kinase B) at its hydrophobic motif (Ser473). In the present study, we report that widely expressed isoforms of unstudied proteins termed Protor-1 (protein observed with Rictor-1) and Protor-2 interact with Rictor and are components of mTORC2. We demonstrate that immunoprecipitation of Protor-1 or Protor-2 results in the co-immunoprecipitation of other mTORC2 subunits, but not Raptor, a specific component of mTORC1. We show that detergents such as Triton X-100 or n-octylglucoside dissociate mTOR and mLST8 from a complex of Protor-1, Sin1 and Rictor. We also provide evidence that Rictor regulates the expression of Protor-1, and that Protor-1 is not required for the assembly of other mTORC2 subunits into a complex. Protor-1 is a novel Rictor-binding subunit of mTORC2, but further work is required to establish its role.

Style APA, Harvard, Vancouver, ISO itp.

41

Jacinto, Estela, Valeria Facchinetti, Dou Liu, Nelyn Soto, Shiniu Wei, Sung Yun Jung, Qiaojia Huang, Jun Qin i Bing Su. "SIN1/MIP1 Maintains rictor-mTOR Complex Integrity and Regulates Akt Phosphorylation and Substrate Specificity". Cell 127, nr 1 (październik 2006): 125–37. http://dx.doi.org/10.1016/j.cell.2006.08.033.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

42

Liu, Pengda, Wenjian Gan, Hiroyuki Inuzuka, Adam S. Lazorchak, Daming Gao, Omotooke Arojo, Dou Liu i in. "Sin1 phosphorylation impairs mTORC2 complex integrity and inhibits downstream Akt signalling to suppress tumorigenesis". Nature Cell Biology 15, nr 11 (27.10.2013): 1340–50. http://dx.doi.org/10.1038/ncb2860.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

43

Tavaluc, Raluca, Howard Herman, Juan Lin i Melin Tan. "Does Reinke’s Edema Grade Determine Premalignant Potential?" Annals of Otology, Rhinology & Laryngology 127, nr 11 (6.09.2018): 812–16. http://dx.doi.org/10.1177/0003489418796529.

Pełny tekst źródła

Streszczenie:

Objective: Reinke’s edema (RE) is a benign disease of the vocal folds with a wide spectrum of clinical severity. We aim to evaluate the clinical impact of RE grade and determine if RE grade correlates with severity of dysplasia and tobacco exposure. Methods: Patients with isolated RE who underwent surgical excision between December 2010 and December 2014 were retrospectively reviewed. The RE grade was determined from archived laryngeal videostroboscopy exams. Pathologic severity of dysplasia, categorized by squamous intraepithelial neoplasia (SIN) classification, and tobacco history were extracted from medical records. Results: Of 95 lesions, 3 (3.16%) were RE grade 1, 33 (34.74%) were RE grade 2, 24 (25.26%) were RE grade 3, and 35 (36.84%) were RE grade 4. Fifty-nine lesions (62.11%) had no dysplasia (SIN0), 19 (20.00%) had mild dysplasia (SIN1), 15 (15.79%) had moderate dysplasia (SIN 2), and 2 (2.11%) had severe dysplasia (SIN3). The 2 patients with severe dysplasia had grade 4 lesions. No statistical correlation was identified between RE grade and the severity of dysplasia. Furthermore, no statistical correlation was seen between tobacco exposure and the severity of dysplasia or the RE grade. Conclusions: Size of RE lesion does not reflect premalignancy. The majority of RE lesions, regardless of size, have little to no premalignant potential. Severe dysplasia/carcinoma in situ may be more likely seen in grade 4 lesions; however, the paucity of severe dysplasia published in RE data and in this cohort preclude any formal inference. Further study of grade 4 lesions is warranted.

Style APA, Harvard, Vancouver, ISO itp.

44

Yang, Q., K. Inoki, T. Ikenoue i K. L. Guan. "Identification of Sin1 as an essential TORC2 component required for complex formation and kinase activity". Genes & Development 20, nr 20 (15.10.2006): 2820–32. http://dx.doi.org/10.1101/gad.1461206.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

45

Kroczynska, Barbara, Gavin T. Blyth, Robert L. Rafidi, Beata Majchrzak-Kita, Lucy Xu, Diana Saleiro, Ewa M. Kosciuczuk i in. "Central Regulatory Role for SIN1 in Interferon γ (IFNγ) Signaling and Generation of Biological Responses". Journal of Biological Chemistry 292, nr 11 (7.02.2017): 4743–52. http://dx.doi.org/10.1074/jbc.m116.757666.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

46

Chang, Xing, Adam S. Lazorchak, Dou Liu i Bing Su. "Sin1 regulates Treg-cell development but is not required for T-cell growth and proliferation". European Journal of Immunology 42, nr 6 (czerwiec 2012): 1639–47. http://dx.doi.org/10.1002/eji.201142066.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

47

Liu, Pengda, Jianping Guo, Wenjian Gan i Wenyi Wei. "Dual phosphorylation of Sin1 at T86 and T398 negatively regulates mTORC2 complex integrity and activity". Protein & Cell 5, nr 3 (31.01.2014): 171–77. http://dx.doi.org/10.1007/s13238-014-0021-8.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

48

Ghosh, D., G. P. Srivastava, D. Xu, L. C. Schulz i R. M. Roberts. "A link between SIN1 (MAPKAP1) and poly(rC) binding protein 2 (PCBP2) in counteracting environmental stress". Proceedings of the National Academy of Sciences 105, nr 33 (7.08.2008): 11673–78. http://dx.doi.org/10.1073/pnas.0803182105.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

49

Liu, Pengda, Wenjian Gan, Hiroyuki Inuzuka, Adam S. Lazorchak, Daming Gao, Omotooke Arojo, Dou Liu i in. "Author Correction: Sin1 phosphorylation impairs mTORC2 complex integrity and inhibits downstream Akt signalling to suppress tumorigenesis". Nature Cell Biology 21, nr 5 (19.02.2019): 662–63. http://dx.doi.org/10.1038/s41556-019-0280-y.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

50

Kaur, Surinder, Barbara Kroczynska, Bhumika Sharma, Antonella Sassano, Ahmet Dirim Arslan, Beata Majchrzak-Kita, Brady L. Stein i in. "Critical Roles for Rictor/Sin1 Complexes in Interferon-dependent Gene Transcription and Generation of Antiproliferative Responses". Journal of Biological Chemistry 289, nr 10 (27.01.2014): 6581–91. http://dx.doi.org/10.1074/jbc.m113.537852.

Pełny tekst źródła

Style APA, Harvard, Vancouver, ISO itp.

Artykuły w czasopismach na temat „Sin1”

Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych