Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P20226 (
TATA-binding protein
)
1,297
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Chronic alcohol consumption is associated with steatohepatitis and cirrhosis, enhancing the risk for hepatocellular carcinoma. RNA polymerase (pol) III transcribes a variety of small, untranslated RNAs, including tRNAs and 5S rRNAs, which determine the biosynthetic capacity of cells. Increased RNA pol III-dependent transcription, observed in transformed cells and human tumors, is required for oncogenic transformation. Given that alcohol consumption increases risk for
liver cancer
, we examined whether alcohol regulates this class of genes. Ethanol induces RNA pol III-dependent transcription in both HepG2 cells and primary mouse hepatocytes in a manner that requires ethanol metabolism and the activation of JNK1. This regulatory event is mediated, at least in part, through the ability of ethanol to induce expression of the TFIIIB components, Brf1, and the
TATA-binding protein
(
TBP
). Induction of
TBP
, Brf1, and RNA pol III-dependent gene expression is driven by enhanced c-Jun expression. Ethanol promotes a marked increase in the direct recruitment of c-Jun to
TBP
, Brf1, and tRNA gene promoters. Chronic alcohol administration in mice leads to enhanced expression of
TBP
, Brf1, tRNA, and 5S rRNA gene transcription in the liver. These alcohol-dependent increases are more pronounced in transgenic animals that express the HCV NS5A protein that display increased incidence of liver tumors. Together, these results identify a new class of genes that are regulated by alcohol through the co-regulation of TFIIIB components and define a central role for c-Jun in this process.
...
PMID:Alcohol induces RNA polymerase III-dependent transcription through c-Jun by co-regulating TATA-binding protein (TBP) and Brf1 expression. 2110 30
Studies on biological functions of N
6
-methyladenosine (m
6
A) modification in mRNA have sprung up in recent years. We find m
6
A can positively regulate the glycolysis of cancer cells. Specifically, m
6
A-sequencing and functional studies confirm that pyruvate dehydrogenase kinase 4 (PDK4) is involved in m
6
A regulated glycolysis and ATP generation. The m
6
A modified 5'UTR of PDK4 positively regulates its translation elongation and mRNA stability via binding with YTHDF1/eEF-2 complex and IGF2BP3, respectively. Targeted specific demethylation of PDK4 m
6
A by dm
6
ACRISPR system can significantly decrease the expression of PDK4 and glycolysis of cancer cells. Further,
TATA-binding protein
(
TBP
) can transcriptionally increase the expression of Mettl3 in cervical cancer cells via binding to its promoter. In vivo and clinical data confirm the positive roles of m
6
A/PDK4 in tumor growth and progression of cervical and
liver cancer
. Our study reveals that m
6
A regulates glycolysis of cancer cells through PDK4.
...
PMID:N
6
-methyladenosine regulates glycolysis of cancer cells through PDK4. 3244 98
