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10.1038/cdd.2016.68 http://scihub22266oqcxt.onion/10.1038/cdd.2016.68 C5071571!5071571 !27391798     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27391798 &cmd=llinks): Failed to open stream: HTTP request failed! 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Expression of Twist2 is controlled by T-cell receptor signaling and determines the survival and death of thymocytes |pdf=|usr=}}{{27391798 }} gab.com Text Expression of Twist2 is controlled by T-cell receptor signaling and determines the survival and death of thymocytes JO: Cell Death Differ http://www.kidney.de/pget.php?&tw=1&pmid=27391798 #FOAvip Self-reactive thymocytes are eliminated by negative selection, whereas competent thymocytes survive by positive selection. The strength of the T-cell receptor (TCR) signal determines the fate of thymocytes undergoing either positive or negative selection. The TCR signal strength is relatively higher in negative selection than in positive selection and induces pro-apoptotic molecules such as Nur77 and Nor-1, which are members of the orphan nuclear receptor family, that then cause TCR-mediated apoptosis. However, at the molecular level, it remains unclear how positive or negative selection is distinguished based on the TCR signal. We found that the expression of Twist2 is differentially regulated in positively and negatively selected thymocytes. In particular, TCR signal strength that elicits positive selection induces Twist2 expression via the Ca(2+)-Cacineurin-NFATc3 pathway, whereas strength of the TCR signal that results in negative selection abolishes NFATc3-dependent Twist2 induction via specific activation of the JNK pathway. Using Twist2-deficient and Twist2 transgenic mice, we also found that Twist2 determines thymocyte sensitivity to TCR-mediated apoptosis by regulating the expression of Nur77 and Nor-1. Twist2 partially retains histone deacetylase 7 (HDAC7) in the nucleus and recruits it to the Nur77 promoter region to repress Nur77 in positively selected thymocytes. Thus our results suggest a molecular mechanism of how thymocytes interpret the strength of the TCR signal and how TCR sensitivity is controlled during thymic selection. Twit Text FOAVip Expression of Twist2 is controlled by T-cell receptor signaling and determines the survival and death of thymocytes ????Cell Death Differ http://www.kidney.de/pget.php?&tw=1&pmid=27391798 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27391798 #FOAvip English Wikipedia <ref>{{Cite pmid|27391798 }}</ref> Expression of Twist2 is controlled by T-cell receptor signaling and determines the survival and death of thymocytes #MMPMID27391798 Oh S ; Oh J ; Lee C ; Oh S ; Jeon S ; Choi J ; Hwang S ; Lee Y ; Lee H ; Seong RH Cell Death Differ 2016[Nov]; 23 (11 ): 1804-1814 PMID27391798 show ga Self-reactive thymocytes are eliminated by negative selection, whereas competent thymocytes survive by positive selection. The strength of the T-cell receptor (TCR) signal determines the fate of thymocytes undergoing either positive or negative selection. The TCR signal strength is relatively higher in negative selection than in positive selection and induces pro-apoptotic molecules such as Nur77 and Nor-1, which are members of the orphan nuclear receptor family, that then cause TCR-mediated apoptosis. However, at the molecular level, it remains unclear how positive or negative selection is distinguished based on the TCR signal. We found that the expression of Twist2 is differentially regulated in positively and negatively selected thymocytes. In particular, TCR signal strength that elicits positive selection induces Twist2 expression via the Ca(2+)-Cacineurin-NFATc3 pathway, whereas strength of the TCR signal that results in negative selection abolishes NFATc3-dependent Twist2 induction via specific activation of the JNK pathway. Using Twist2-deficient and Twist2 transgenic mice, we also found that Twist2 determines thymocyte sensitivity to TCR-mediated apoptosis by regulating the expression of Nur77 and Nor-1. Twist2 partially retains histone deacetylase 7 (HDAC7) in the nucleus and recruits it to the Nur77 promoter region to repress Nur77 in positively selected thymocytes. Thus our results suggest a molecular mechanism of how thymocytes interpret the strength of the TCR signal and how TCR sensitivity is controlled during thymic selection. |*Apoptosis [MESH] |*Signal Transduction [MESH] |Animals [MESH] |Calcineurin/metabolism [MESH] |Cell Survival [MESH] |DNA-Binding Proteins/metabolism [MESH] |Histone Deacetylases/metabolism [MESH] |JNK Mitogen-Activated Protein Kinases/metabolism [MESH] |MEF2 Transcription Factors/metabolism [MESH] |Mice, Inbred C57BL [MESH] |NFATC Transcription Factors/metabolism [MESH] |Nerve Tissue Proteins/metabolism [MESH] |Nuclear Receptor Subfamily 4, Group A, Member 1/metabolism [MESH] |Protein Binding [MESH] |Receptors, Antigen, T-Cell/*metabolism [MESH] |Receptors, Steroid/metabolism [MESH] |Receptors, Thyroid Hormone/metabolism [MESH] |Repressor Proteins/deficiency/*metabolism [MESH] |Thymocytes/*cytology/*metabolism [MESH] |Twist-Related Protein 1/deficiency/*metabolism [MESH]Expression of Twist2 is controlled by T-cell receptor signaling and de(epmc).pdf DeepDyve Pubget Overpricing