Добірка наукової літератури з теми "TGFGIp"
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Статті в журналах з теми "TGFGIp"
Anandalakshmi, Venkatraman, Guillaume Hochart, David Bonnel, Jonathan Stauber, Shigeto Shimmura, Rajamani Lakshminarayanan, Konstantin Pervushin, and Jodhbir S. Mehta. "Targeted Expression of TGFBIp Peptides in Mouse and Human Tissue by MALDI-Mass Spectrometry Imaging." Separations 8, no. 7 (July 3, 2021): 97. http://dx.doi.org/10.3390/separations8070097.
Повний текст джерелаMiyakawa, Ayumi A., Thais Girão-Silva, Jose E. Krieger, and Elazer R. Edelman. "Rapamycin activates TGF receptor independently of its ligand: implications for endothelial dysfunction." Clinical Science 132, no. 4 (February 16, 2018): 437–47. http://dx.doi.org/10.1042/cs20171457.
Повний текст джерелаPereira, Marcelo de Souza Fernandes, Yasemin Sezgin, Aarohi Thakkar та Dean Anthony Lee. "Tgfβ-Imprinting Decrease CD38 Expression and Lead to Metabolic Reprogramming on Primary NK Cell". Blood 136, Supplement 1 (5 листопада 2020): 4. http://dx.doi.org/10.1182/blood-2020-143085.
Повний текст джерелаLee, In-Chul, and Jong-Sup Bae. "Suppressive Effects of Sulforaphane on TGFBIp-mediated Sepsis." Natural Product Communications 12, no. 10 (October 2017): 1934578X1701201. http://dx.doi.org/10.1177/1934578x1701201026.
Повний текст джерелаKim, Ha-Jeong, Suyeon Rhe, and Haeuk Jung. "Platelet TGFBIp induces foam cell formation after platelet phagocytosis." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 206.26. http://dx.doi.org/10.4049/jimmunol.198.supp.206.26.
Повний текст джерелаKim, Ha-Jeong, Pan-Kyung Kim, Sang Mun Bae, Hye-Nam Son, Debraj Singh Thoudam, Jung-Eun Kim, Byung-Heon Lee, Rang-Woon Park та In-San Kim. "Transforming growth factor-β–induced protein (TGFBIp/β ig-h3) activates platelets and promotes thrombogenesis". Blood 114, № 25 (10 грудня 2009): 5206–15. http://dx.doi.org/10.1182/blood-2009-03-212415.
Повний текст джерелаJeong, Seongdo, Sae-Kwang Ku, and Jong-Sup Bae. "Anti-inflammatory effects of pelargonidin on TGFBIp-induced responses." Canadian Journal of Physiology and Pharmacology 95, no. 4 (April 2017): 372–81. http://dx.doi.org/10.1139/cjpp-2016-0322.
Повний текст джерелаPark, Hee Ho, Hong Nam Kim, Hyelim Kim, Youngbum Yoo, Hyosoo Shin, Eun Young Choi, Jong-Sup Bae, and Wonhwa Lee. "Acetylated K676 TGFBIp as a severity diagnostic blood biomarker for SARS-CoV-2 pneumonia." Science Advances 6, no. 31 (July 2020): eabc1564. http://dx.doi.org/10.1126/sciadv.abc1564.
Повний текст джерелаNam, Sang Min, Yong-Sun Maeng, Eung Kweon Kim, Kyoung Yul Seo, and Helen Lew. "Ex Vivo Expansion of Human Limbal Epithelial Cells Using Human Placenta-Derived and Umbilical Cord-Derived Mesenchymal Stem Cells." Stem Cells International 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/4206187.
Повний текст джерелаSørensen, Charlotte S., Kasper Runager, Carsten Scavenius, Morten M. Jensen, Nadia S. Nielsen, Gunna Christiansen, Steen V. Petersen, Henrik Karring, Kristian W. Sanggaard, and Jan J. Enghild. "Fibril Core of Transforming Growth Factor Beta-Induced Protein (TGFBIp) Facilitates Aggregation of Corneal TGFBIp." Biochemistry 54, no. 19 (May 6, 2015): 2943–56. http://dx.doi.org/10.1021/acs.biochem.5b00292.
Повний текст джерелаДисертації з теми "TGFGIp"
Wang, Feng. "The role of TGFBI in development and cancer." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610043.
Повний текст джерелаSchwanekamp, Jennifer A. "Dissecting the Roles of Periostin and TGFBI in Cardiovascular Disease." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1504803264229101.
Повний текст джерелаDixon, James Edward. "Arkadia Family Ubiquitin-Ligases in TGFp Signalling." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.486282.
Повний текст джерелаRuiz, Maxime. "Le TGFβI dans la physiopathologie de l'arthrose et son rôle dans l'effet thérapeutique des cellules souches mésenchymateuses". Thesis, Montpellier, 2018. http://www.theses.fr/2018MONTT008/document.
Повний текст джерелаOsteoarthritis (OA) is the most common form of joint diseases without curative treatments. The disease is mainly characterized by the degradation of articular cartilage which is associated with other pathological changes in joint tissues. In this context, mesenchymal stem cells (MSC) have demonstrated a therapeutic effect. In order to identify new mediators involved in articular homeostasis, we analyzed MSC secretome, focusing on the transforming growth factor β (TGFβ) members, a central pathway dysregulated in OA.This approach allows us to identify the TGFβ induced protein (TGFβI or βIGH3). In the present study, we evaluated its role in the differentiation of MSC and compared its expression in articular tissues from OA patients and healthy donors.We highlight the importance of TGFβI in the regulation of differentiation of MSC towards bone and cartilage. We also demonstrate its dysregulation at both transcript and protein level in cartilage, bone and MSC from OA patients. We then evaluated its role in the therapeutic effect of MSC in vitro and in vivo and demonstrated that its decreased expression in MSC is associated with a loss of their therapeutic effect in OA models. The chondroprotective effect of TGFβI is associated with an inhibition of bone remodeling and calcification of soft articular tissues.Together, our results highlight the importance of the TGFβ pathway, and specially of TGFβI regulation, in joint homeostasis. Moreover, our work demonstrates its role in the therapeutic effect of MSC, suggesting that its dysregulation in OA MSC could lead to a decreased regenerative potential
Touma, Dona. "Molecular differences in sporadic breast cancer in young women (≤ 35-year old) : analysis of TGFBI, DDB2 and MCM5." Thesis, University of Leicester, 2011. http://hdl.handle.net/2381/9164.
Повний текст джерелаMorazzo, Sofia Faes. "A potencial função do nodal na endometrose da égua." Master's thesis, Universidade de Lisboa, Faculdade de Medicina Veterinária, 2017. http://hdl.handle.net/10400.5/14039.
Повний текст джерелаAlguns membros da superfamília do TGFβ, tais como o Nodal e o TGFβ1, têm um papel importante na reprodução da égua, sendo que a sua disfunção pode contribuir para patologias uterinas. A endometrose é uma doença degenerativa em que o endométrio normal vai sendo substituído por tecido fibrótico. O objectivo deste estudo consistiu em avaliar: (i) como o Nodal pode influenciar o nível de mRNA dos recetores da PGE2 (EP2; EP4), do TGFβ1 (ALK5; TGFRII), e os próprios (ALK4; ALK7), e ainda, a secreção de prostaglandinas (PGs; PGE2; PGF2α) no endométrio equino; e (ii) como a fase do ciclo éstrico e grau de endometrose pode influenciar estas vias. Endométrios da fase folicular (FF; n=6) e da fase lútea (FL; n=6) foram classificados de acordo com o sistema de Kenney e Doig em categorias I e IIA (n=7), ou IIB e III (n=5). Os explantes foram incubados (24h; 37ºC, 5% CO2) com TNFα, ocitocina ou Nodal (0.1;1;10 ng/mL). A expressão de mRNA foi avaliada por qRT-PCR e a medição de prostaglandinas por ELISA. Em endométrios de categoria I/IIA, o Nodal inibiu a expressão génica de EP2, EP4 e ALK4 e estimulou a de TGFRII, em ambas as fases do ciclo éstrico; e estimulou também os níveis de mRNA de ALK5 e ALK7, apenas na FL. Em endométrios de categoria IIB/III, o Nodal estimulou os níveis de mRNA de EP2, EP4 e ALK5, na FF, e de ALK4 e ALK7, na FL, embora tenha inibido TGFRII e ALK4, na FF, e EP2, EP4, ALK5 e TGFRII na FL. O Nodal na concentração testada mais baixa (0.1ng/mL) estimulou a produção de PGE2 na FF e FL, enquanto que numa concentração superior a inibiu na FF (1ng/mL). A produção de PGF2α foi estimulada na FL com Nodal (0.1 e 10ng/mL). Concluindo, o Nodal parece estar envolvido na endometrose da égua, por afetar negativamente a sinalização da PGE2 anti-fibrótica e positivamente a da citocina pró-fibrótica TGFβ1 e a produção de PGF2α.
ABSTRACT - THE POTENCIAL ROLE OF NODAL IN MAR ENDOMETROSIS - Members of TGFβ superfamily, as Nodal and TGFβ1, have an important role in mare´s reproduction, and as such, their dysfunction may contribute for uterine pathologies. Endometrosis is a degenerative process with a switch of normal endometrium to fibrotic tissue. The aim of the study was to assess: (i) how Nodal may influence the receptors of PGE2 (EP2; EP4), TGFβ1 (ALK5; TGFRII), and its own (ALK4; ALK7) mRNA level and prostaglandin (PG) secretion in equine endometrium; and (ii) estrous cycle and endometrosis influence on these vias. Endometria from follicular (FP; n=6) and mid luteal phases (MLP; n=6) were classified in Kenney and Doig´s categories (cat) I and IIA (n=7), or IIB and III (n=5). Endometrium explants were incubated (24h; 37ºC, 5% CO2) with TNF, oxytocin or Nodal (0.1, 1; 10ng/mL). The mRNA expression was assessed by qRT-PCR and ELISA was used for PG measurement. In cat I/IIA endometria, Nodal down-regulated EP2, EP4 and ALK4 mRNA expression and up-regulated TGFRII in both FP and MLP; and ALK5 and ALK7 only in MLP. In cat IIB/III, Nodal up-regulated mRNA levels of EP2, EP4 and ALK5 in FP, and ALK4 and ALK7 in MLP, whereas it inhibited TGFRII and ALK4 in FP, and EP2, EP4, ALK5 and TGFRII in MLP. Nodal (0.1ng/mL) stimulated PGE2 production in both FF and FL, while at a higher concentration (1ng/mL) it decreased PGE2 in FP. The production of PGF2α increased in MLP with Nodal stimulation (at 0.1 and 10ng/mL). In conclusion, Nodal may be involved in endometrosis in the mare, by impairment of anti-fibrotic PGE2 and pro-fibrotic TGFβ1 signaling pathways and increasing PGF2α production.
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Ween, Miranda Peggy. "The biological role of extracellular matrix in ovarian cancer metastasis." Thesis, 2010. http://hdl.handle.net/2440/65056.
Повний текст джерелаThesis (Ph.D.) -- University of Adelaide, School of Paediatrics and Reproduction Health, 2010
Peng, Bai-Jing, and 彭百竟. "Efficient Microwave-Assisted Palladium-Catalyzed Allylation of 2,3-Disubstituted Indoles with Allylic Alcohols." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/tgfg45.
Повний текст джерела高雄醫學大學
藥學研究所
102
A principal goal of organometallic chemistry is the catalytic synthesis of organic compounds by using the chemistry of organic ligands covalently bound to transition metals. The palladium-catalyzed allylation of N-nucleophiles was an established and efficient method, which has been widely applied to organic chemistry. Utilizing the prevalence of indole nucleus in biologically active compounds, the direct C3-functionalization or N-functionalization of 2,3-disubstituted indoles represent an important problem. In this study, the palladium-catalyzed 2,3-disubstitued indoles with allylic alcohols in benzene was investigated under various conditions. Furthermore, microwave has been widely applied to shorten reaction time in organic synthesis. Herein, we develop a new highly selective method. This method provide particularly convenient, efficient, and selective.
De, la Mare Jo-Anne, Tamarin Jurgens, and Adrienne Lesley Edkins. "Extracellular Hsp90 and TGFP regulate adhesion, migration and anchorage independent growth in a paired colon cancer cell line model." 2017. http://hdl.handle.net/10962/59920.
Повний текст джерелаЧастини книг з теми "TGFGIp"
Becker, Jürgen. "Pediatric Neuroblastoma: Role of TGFBI (Keratoepithelin)." In Pediatric Cancer, 229–36. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2418-1_23.
Повний текст джерелаHei, Tom K., Yongliang Zhao, Hongning Zhou, and Vladimir Ivanov. "Mechanism of Radiation Carcinogenesis: Role of the TGFBI Gene and the Inflammatory Signaling Cascade." In Advances in Experimental Medicine and Biology, 163–70. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0254-1_13.
Повний текст джерелаHinz, Steffen C., Adrian Elter, Julius Grzeschik, Jan Habermann, Bastian Becker, and Harald Kolmar. "Simplifying the Detection of Surface Presentation Levels in Yeast Surface Display by Intracellular tGFP Expression." In Methods in Molecular Biology, 211–22. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-4939-9853-1_12.
Повний текст джерелаStenvang, Marcel, Maria Andreasen, Jan Johannes Enghild, and Daniel E. Otzen. "The Molecular Basis For TGFBIp-Related Corneal Dystrophies." In Bio-nanoimaging, 179–88. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-394431-3.00016-x.
Повний текст джерелаRöcken, C., A. Roessner, J. Rüschoff, and B. Stix. "Corneal Dystrophy Caused by a Novel Mutation of the TGFBI Gene." In Amyloid and Amyloidosis, 438–39. CRC Press, 2004. http://dx.doi.org/10.1201/9781420037494.ch150.
Повний текст джерела"Corneal Dystrophies." In Medical Atlas of Cornea and External Diseases in Middle Eastern Populations, 251–64. IGI Global, 2022. http://dx.doi.org/10.4018/978-1-7998-6937-5.ch008.
Повний текст джерелаStix, B., J. Rüschoff, A. Roessner, and C. Röcken. "Corneal Dystrophy Caused by a Novel Mutation of the TGFBI Gene: A Case Report." In Amyloid and Amyloidosis, 438–39. CRC Press, 2004. http://dx.doi.org/10.1201/9781420037494-156.
Повний текст джерелаТези доповідей конференцій з теми "TGFGIp"
Seo, Jun-Young, Hae Uk Jung, Hye-Nam Son, Soyoun Kim, Eunsung Jun, Ju-Ock Nam, Jung-Eun Kim, and In-San Kim. "Abstract 11: Absence of TGFBI favors tumor angiogenesis." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-11.
Повний текст джерелаRuiz, Maxime, Marie Maumus, Karine Toupet, Guillaume Fonteneau, Yves-Marie Pers, Xavier Houard, Francis Berenbaum, Christian Jorgensen та Danièle Noël. "04.03 Tgfβ-induced protein (tgfβi) is dysregulated in osteoarthritis". У 37th European Workshop for Rheumatology Research 2–4 March 2017 Athens, Greece. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2016-211051.3.
Повний текст джерелаNayeem, N. M., and J. E. Rice. "A New Approach to Online Testing of TGFSOP-based Ternary Toffoli Circuits." In 2012 IEEE 42nd International Symposium on Multiple-Valued Logic (ISMVL). IEEE, 2012. http://dx.doi.org/10.1109/ismvl.2012.57.
Повний текст джерелаJiao, Yunjuan, Weixing Zhao, Xin Dong, Xiaoyu Yang, Zheying Zhang, Yongxia Wang, Jing Cui, Zhiqiang Qin, Wancai Yang та Wancai Yang. "Abstract 4689: The alterations and significance of hMLH1 and TGFβII receptor expression during esophageal carcinogenesis." У Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-4689.
Повний текст джерелаBragado, Paloma, Yeriel Estrada, Maria Soledad Sosa, Denis M. Schewe, Carla Capobianco, Kateri Moore, Hernan G. Farina та Julio Aguirre-Ghiso. "Abstract 5234: Microenvironmental signals dictate disseminated tumor cells (DTCs) fate through regulation of TGFβII and p38α". У Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5234.
Повний текст джерелаRudra-Ganguly, Nandini, Daulet Satpayev, Christine Lowe, Liping Hu, Bally Randhawa, Mi Sook Chang, Alla Verlinsky, et al. "Abstract 1086: Discoidin domain receptor 1 contributes to tumorigenesis through modulation of TGFBI expression." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1086.
Повний текст джерелаBissey, Pierre-Antoine, Jeff W. Bruce, Jacqueline Law, Kenneth W. Yip, and Fei-Fei Liu. "Abstract 5038: The repression of the extracellular matrix protein TGFBI induces chemoresistance in nasopharyngeal carcinoma." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-5038.
Повний текст джерелаLee, Jong-Joo, Joo-Hong Park, Keunhee Park, Min-Ji Song, Wook-Jin Yang, and Hyoung-Pyo Kim. "Abstract 2211: Accessible chromatin structure permits factors Sp1 and Sp3 to regulate human TGFBI gene expression." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2211.
Повний текст джерелаLiu, Yen-Nien, Wei-Yu Chen, Yuan-Chin Tsai, Hsiu-Lien Yeh, Florent Suau, and Jiaoti Huang. "Abstract A031: Androgen deprivation therapy-induced TGFBI signaling promotes EMT and bone metastasis of prostate cancer." In Abstracts: AACR Special Conference: Prostate Cancer: Advances in Basic, Translational, and Clinical Research; December 2-5, 2017; Orlando, Florida. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.prca2017-a031.
Повний текст джерелаMuramatsu, Tomoki, Taku Sato, Minoru Tanabe, and Johji Inazawa. "Abstract 163: Identification and characterization of TGFBI in circulating tumor cell subline from pancreatic cancer cell line." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-163.
Повний текст джерелаЗвіти організацій з теми "TGFGIp"
Anderson, Ryan M. Functional Analysis of TGF-alpha/beta Regulated Protein (TGFRP) in Breast Cancer Angiogenesis. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada412099.
Повний текст джерелаXu, Mingna, Yaru Guo, and Song Yang. Prognostic and Clinicopathological Significance of TGFBI Expression in Cancer Patients: A Meta-Analysis and Bioinformatics Validation. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2021. http://dx.doi.org/10.37766/inplasy2021.10.0089.
Повний текст джерела