TTC39B destabilizes retinoblastoma protein promoting hepatic lipogenesis in a sex-specific fashion

2021 ◽  
Author(s):  
Joanne Hsieh ◽  
Matthew M. Molusky ◽  
Kristin M. McCabe ◽  
Panagiotis Fotakis ◽  
Tong Xiao ◽  
...  
Keyword(s):  
Retinoblastoma Protein ◽  
Hepatic Lipogenesis

The role of microRNA-33 as a key regulator in hepatic lipogenesis signaling and a potential serological biomarker for NAFLD with excessive dietary fructose consumption in C57BL/6N mice

2021 ◽  
Author(s):  
Jeong Hoon Pan ◽  
Hanvit Cha ◽  
Jingsi Tang ◽  
Seoyoon Lee ◽  
Suk Hee Lee ◽  
...  
Keyword(s):  
Fatty Liver ◽  
Blood Stream ◽  
Hepatic Lipogenesis ◽  
Dietary Fructose

Fructose-induced hepatic miR-33 suppression lead to fatty liver via upregulation of SREBP1. Additionally, fructose-induced hepatic ferroptosis may cause a spill-over of miR-33 into blood stream, which could be a potential serological biomarker for fructose-induced NAFLD.

scholarly journals Retinoblastoma protein reverses DNA bending by transcription factor E2F.

1994 ◽  
Vol 269 (9) ◽  
pp. 6999-7005 ◽  
Author(s):  
H.E. Huber ◽  
P.J. Goodhart ◽  
P.S. Huang
Keyword(s):  
Transcription Factor ◽  
Dna Bending ◽  
Retinoblastoma Protein ◽  
Transcription Factor E2f

scholarly journals Decreased SUMOylation of the retinoblastoma protein in keratinocytes during the pathogenesis of vitiligo

2018 ◽  
Author(s):  
Miaoni Zhou ◽  
Fuquan Lin ◽  
Wen Xu ◽  
Rong Jin ◽  
Aie Xu
Keyword(s):  
Retinoblastoma Protein

Proline and hepatic lipogenesis

1984 ◽  
Vol 798 (3) ◽  
pp. 368-373 ◽  
Author(s):  
M SUGDEN ◽  
D WATTS ◽  
P WEST ◽  
T NORMANPALMER
Keyword(s):  
Hepatic Lipogenesis

The p53-mediated sensitivity of cancer cells to chemotherapeutic agents is conditioned by the status of the retinoblastoma protein

2009 ◽  
Vol 219 (3) ◽  
pp. 373-382 ◽  
Author(s):  
Massimo Derenzini ◽  
Elisa Brighenti ◽  
Giulio Donati ◽  
Manuela Vici ◽  
Claudio Ceccarelli ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Retinoblastoma Protein ◽  
Chemotherapeutic Agents ◽  
The Status

The p38MAPK signaling pathway regulates neuronal apoptosis through the phosphorylation of the retinoblastoma protein

2009 ◽  
Vol 54 (2) ◽  
pp. 99-105 ◽  
Author(s):  
Marc Yeste-Velasco ◽  
Jaume Folch ◽  
Mercè Pallàs ◽  
Antoni Camins
Keyword(s):  
Signaling Pathway ◽  
Neuronal Apoptosis ◽  
Retinoblastoma Protein ◽  
P38mapk Signaling

scholarly journals BRG1 Controls the Activity of the Retinoblastoma Protein via Regulation of p21CIP1/WAF1/SDI

2004 ◽  
Vol 24 (3) ◽  
pp. 1188-1199 ◽  
Author(s):  
Hyeog Kang ◽  
Kairong Cui ◽  
Keji Zhao
Keyword(s):  
Transcriptional Repression ◽  
Cell Cycle Progression ◽  
Target Genes ◽  
Cellular Proliferation ◽  
Growth Arrest ◽  
Retinoblastoma Protein ◽  
Direct Interaction ◽  
Physical Interaction ◽  
Cdk Inhibitor ◽  
Regulation Of Cell Cycle

ABSTRACT The ubiquitous mammalian chromatin-remodeling SWI/SNF-like BAF complexes play critical roles in tumorigenesis. It was suggested that the direct interaction of BRG1 with the retinoblastoma protein pRB is required for regulation of cell cycle progression by pRB. We present evidence that the BRG1-containing complexes regulate the expression of the cdk inhibitor p21CIP1/WAF1/SDI. Furthermore, we show that the physical interaction between BRG1 and pRB is not required for induction of cell growth arrest and transcriptional repression of E2F target genes by pRB. Instead, BRG1 activates pRB by inducing its hypophosphorylation through up-regulation of the cdk inhibitor p21. The hypophosphorylation of pRB is reinforced by down-regulation of critical components, including cdk2, cyclin E, and cyclin D, in the pRB regulatory network. We demonstrate that up-regulation of p21 by BRG1 is necessary to induce formation of flat cells, growth arrest, and finally, cell senescence. Our results suggest that the BRG1-containing complexes control cellular proliferation and senescence by modulating the pRB pathway via multiple mechanisms.

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