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Increased MAT1A expression is associated with recurrence in hepatocellular carcinoma.
interplay between MATalpha1, c-Myc (show MYC Proteins), and Maf (show MAF Proteins) proteins, and their deregulation during chronic cholestasis may facilitate cholangiocarcinoma oncogenesis
Of the 22 single nucleotide polymorphisms studied, the rs8193 polymorphism lying in the micro-RNA binding site of 3'-UTR of CD44 (show CD44 Proteins) was significantly (P=.0270) associated with RT-induced adverse skin reactions. Generalized multifactor dimensionality reduction analysis showed significant (P=.0107) gene-gene interactions between MAT1A and CD44 (show CD44 Proteins).
A compound mutation of the methionine adenosyltransferase 1A (MAT1A) gene, c.345delA and c.529C>T, was identified in the patient, and His father and mother were found to be heterozygous for the c.345delA mutation and c.529C>T mutation, respectively.
S-adenosyl-L-methionine (show AS3MT Proteins) diminishes hepatitis C virus expression by altering MAT1A/2A signaling in hepatocytes.
5-Aza-CdR (show RUNX1T1 Proteins) showed no effects on MAT2A (show MAT2A Proteins) methylation.
The mutations in the other 10 patients showed autosomal recessive inheritance and included eight novel MAT1A mutations.
Liver-specific isoenzyme MAT1A is genetically linked with an inborn metabolic disorder of hypermethioninemia, as well as a ubiquitously expressed isoenzyme MAT2A (show MAT2A Proteins), whose enzymatic activity is regulated by an associated subunit MAT2B (show MAT2B Proteins).
Methionine adenosyltransferase I/III deficiency is caused by mutations in the MAT1A gene. (Review)
upregulation of miR (show MLXIP Proteins)-664, miR (show MLXIP Proteins)-485-3p, and miR (show MLXIP Proteins)-495 contributes to lower MAT1A expression in HCC (show FAM126A Proteins), and enhanced tumorigenesis may provide potential targets for HCC (show FAM126A Proteins) therapy.
MAT1A is required for normal VLDL assembly and plasma lipid homeostasis in mice. Impaired VLDL synthesis, mainly due to SAMe deficiency, contributes to NAFLD development in MAT1A-KO mice.
DUSP1 (show DUSP1 Proteins) mRNA and protein levels are lower in Mat1a knockout livers and fall rapidly in cultured hepatocytes.
Spontaneous oxidative stress and liver tumors in mice lacking methionine adenosyltransferase 1A
MAT1A knockout hepatocytes have more baseline DNA synthesis but no mitogenic response to hepatocyte growth factor (show HGF Proteins). MAT1A-produced SAMe has a major role in ERK (show EPHB2 Proteins) signaling & cyclin D1 (show CCND1 Proteins) regulation during liver regeneration & mitogenic signal response.
Mat1a(-/-) mice have expansion of liver stem cells as they age. These cells have increased expression of several oncogenes and are tumorigenic in vivo.
C/EBPbeta (show CEBPB Proteins) plays an important role in epigenetic regulation of the mature hepatic gene MAT1A
By 1 month of age, genomic instability increases in livers of Mat1a knockout mice, possibly due to reduced APEX1 (show APEX1 Proteins) levels
CD133(+)CD45(-) oval cells isolated from premalignant 16-month-old Mat1a(-/-) mice demonstrated significant resistance to transforming growth factor-beta-induced apoptosis compared to CD133(-) cells.
This gene catalyzes a two-step reaction that involves the transfer of the adenosyl moiety of ATP to methionine to form S-adenosylmethionine and tripolyphosphate, which is subsequently cleaved to PPi and Pi. S-adenosylmethionine is the source of methyl groups for most biological methylations. The encoded protein is found as a homotetramer (MAT I) or a homodimer (MAT III) whereas a third form, MAT II (gamma), is encoded by the MAT2A gene. Mutations in this gene are associated with methionine adenosyltransferase deficiency.
, S-adenosylmethionine synthase isoform type-1
, S-adenosylmethionine synthetase isoform type-1
, adoMet synthase 1
, adoMet synthetase 1
, methionine adenosyltransferase 1
, methionine adenosyltransferase I/III
, S - adenosylmethionine synthetase