scholarly journals Cell Density Sensing Alters TGF-β Signaling in a Cell-Type-Specific Manner, Independent from Hippo Pathway Activation

2015 ◽  
Vol 32 (5) ◽  
pp. 640-651 ◽  
Author(s):  
Flore Nallet-Staub ◽  
Xueqian Yin ◽  
Cristèle Gilbert ◽  
Véronique Marsaud ◽  
Saber Ben Mimoun ◽  
...  
Keyword(s):  
Cell Density ◽  
Hippo Pathway ◽  
Cell Type ◽  
Pathway Activation ◽  
Specific Manner ◽  
A Cell ◽  
Cell Type Specific

Abstract LB-028: Cell density sensing alters TGF-beta signaling in a cell type-specific manner, independent from Hippo pathway activation

2015 ◽  
Author(s):  
Flore Nallet-Staub ◽  
Xueqian Yin ◽  
Cristèle Gilbert ◽  
Véronique Marsaud ◽  
Saber Ben Mimoun ◽  
...  
Keyword(s):  
Cell Density ◽  
Hippo Pathway ◽  
Tgf Beta ◽  
Cell Type ◽  
Pathway Activation ◽  
Specific Manner ◽  
A Cell ◽  
Cell Type Specific

scholarly journals Rel Induces Interferon Regulatory Factor 4 (IRF-4) Expression in Lymphocytes

2000 ◽  
Vol 191 (8) ◽  
pp. 1281-1292 ◽  
Author(s):  
Raelene J. Grumont ◽  
Steve Gerondakis
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Nuclear Factor Κb ◽  
Wild Type ◽  
Cell Type ◽  
Regulatory Factor ◽  
Specific Manner ◽  
A Cell ◽  
Cell Type Specific ◽  
Interferon Regulatory Factor 4

In lymphocytes, the Rel transcription factor is essential in establishing a pattern of gene expression that promotes cell proliferation, survival, and differentiation. Here we show that mitogen-induced expression of interferon (IFN) regulatory factor 4 (IRF-4), a lymphoid-specific member of the IFN family of transcription factors, is Rel dependent. Consistent with IRF-4 functioning as a repressor of IFN-induced gene expression, the absence of IRF-4 expression in c-rel−/− B cells coincided with a greater sensitivity of these cells to the antiproliferative activity of IFNs. In turn, enforced expression of an IRF-4 transgene restored IFN modulated c-rel−/− B cell proliferation to that of wild-type cells. This cross-regulation between two different signaling pathways represents a novel mechanism that Rel/nuclear factor κB can repress the transcription of IFN-regulated genes in a cell type–specific manner.

PLAG1 enhances the stemness profiles of acinar cells in normal human salivary glands in a cell type-specific manner

2020 ◽  
Vol 62 (1) ◽  
pp. 99-106 ◽  
Author(s):  
Yuriko Goto ◽  
Miho Ibi ◽  
Hirotaka Sato ◽  
Junichi Tanaka ◽  
Rika Yasuhara ◽  
...  
Keyword(s):  
Salivary Glands ◽  
Acinar Cells ◽  
Cell Type ◽  
Specific Manner ◽  
A Cell ◽  
Normal Human ◽  
Cell Type Specific

scholarly journals Fibronectin signals through integrin α5β1 to regulate cardiovascular development in a cell type-specific manner

2015 ◽  
Vol 407 (2) ◽  
pp. 195-210 ◽  
Author(s):  
Dongying Chen ◽  
Xia Wang ◽  
Dong Liang ◽  
Julie Gordon ◽  
Ashok Mittal ◽  
...  
Keyword(s):  
Cardiovascular Development ◽  
Cell Type ◽  
Integrin Α5β1 ◽  
Specific Manner ◽  
A Cell ◽  
Cell Type Specific

scholarly journals miR-27 and miR-125 Distinctly Regulate Muscle-Enriched Transcription Factors in Cardiac and Skeletal Myocytes

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Estefania Lozano-Velasco ◽  
Jennifer Galiano-Torres ◽  
Alvaro Jodar-Garcia ◽  
Amelia E. Aranega ◽  
Diego Franco
Keyword(s):  
Transcription Factors ◽  
Cardiac Development ◽  
Protein Translation ◽  
Cell Type ◽  
Atrial Cardiomyocytes ◽  
Skeletal Myocytes ◽  
Specific Manner ◽  
A Cell ◽  
Cell Type Specific

MicroRNAs are noncoding RNAs of approximately 22–24 nucleotides which are capable of interacting with the 3′ untranslated region of coding RNAs (mRNAs), leading to mRNA degradation and/or protein translation blockage. In recent years, differential microRNA expression in distinct cardiac development and disease contexts has been widely reported, yet the role of individual microRNAs in these settings remains largely unknown. We provide herein evidence of the role of miR-27 and miR-125 regulating distinct muscle-enriched transcription factors. Overexpression of miR-27 leads to impair expression ofMstnandMyocdin HL1 atrial cardiomyocytes but not in Sol8 skeletal muscle myoblasts, while overexpression of miR-125 resulted in selective upregulation ofMef2din HL1 atrial cardiomyocytes and downregulation in Sol8 cells. Taken together our data demonstrate that a single microRNA, that is, miR-27 or miR-125, can selectively upregulate and downregulate discrete number of target mRNAs in a cell-type specific manner.

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