Results 21 to 30 of about 3,813 (143)

Methionine adenosyltransferases in liver cancer [PDF]

open access: yesWorld Journal of Gastroenterology, 2019
Methionine adenosyltransferases (MATs) are essential enzymes for life as they produce S-adenosylmethionine (SAMe), the biological methyl donor required for a plethora of reactions within the cell. Mammalian systems express two genes, MAT1A and MAT2A, which encode for MATα1 and MATα2, the catalytic subunits of the MAT isoenzymes, respectively.
Murray, Ben   +4 more
openaire   +3 more sources

Regulation of Mammalian Liver Methionine Adenosyltransferase [PDF]

open access: yesThe Journal of Nutrition, 2002
S-adenosylmethionine (SAM) is an essential metabolite in all cells. SAM is the most important biological methyl group donor and is a precursor in the synthesis of polyamines. Methionine adenosyltransferase (MAT; EC 2.5.1.6) catalyzes the only known SAM biosynthetic reaction from methionine and ATP.
Latasa, M.U. (María Ujué)   +10 more
openaire   +3 more sources

Structure-function relationships in methionine adenosyltransferases [PDF]

open access: yesCellular and Molecular Life Sciences, 2008
Methionine adenosyltransferases (MATs) are the family of enzymes that synthesize the main biological methyl donor, S-adenosylmethionine. The high sequence conservation among catalytic subunits from bacteria and eukarya preserves key residues that control activity and oligomerization, which is reflected in the protein structure.
G D, Markham, M A, Pajares
openaire   +2 more sources

Leishmania donovani methionine adenosyltransferase [PDF]

open access: yesEuropean Journal of Biochemistry, 2002
Junta de Castilla y ...
Pérez Pertejo, Maria Yolanda   +6 more
openaire   +5 more sources

Hyperphosphorylation of hepatic proteome characterizes nonalcoholic fatty liver disease in S-adenosylmethionine deficiency

open access: yesiScience, 2023
Summary: Methionine adenosyltransferase 1a (MAT1A) is responsible for hepatic S-adenosyl-L-methionine (SAMe) biosynthesis. Mat1a−/− mice have hepatic SAMe depletion, develop nonalcoholic steatohepatitis (NASH) which is reversed with SAMe administration ...
Aaron E. Robinson   +16 more
doaj   +1 more source

Characterisation of methionine adenosyltransferase from Mycobacterium smegmatis and M. tuberculosis

open access: yesBMC Microbiology, 2003
Background Tuberculosis remains a serious world-wide health threat which requires the characterisation of novel drug targets for the development of future antimycobacterials.
Knodel Marvin H, Berger Bradley J
doaj   +1 more source

Knockdown of METTL16 disrupts learning and memory by reducing the stability of MAT2A mRNA

open access: yesCell Death Discovery, 2022
N6-methyladenosine (m6A) is abundant in the mammalian brain and is considered to have a wide range of effects on learning and memory. Here, we found that the upregulated methyltransferase-like protein 16 (METTL16) in the hippocampal tissues of Morris ...
Runjiao Zhang   +10 more
doaj   +1 more source

Dietary folate drives methionine metabolism to promote cancer development by stabilizing MAT IIA

open access: yesSignal Transduction and Targeted Therapy, 2022
Folic acid, served as dietary supplement, is closely linked to one-carbon metabolism and methionine metabolism. Previous clinical evidence indicated that folic acid supplementation displays dual effect on cancer development, promoting or suppressing ...
Jin-Tao Li   +15 more
doaj   +1 more source

S-Adenosylmethionine Synthesis Is Regulated by Selective N6-Adenosine Methylation and mRNA Degradation Involving METTL16 and YTHDC1

open access: yesCell Reports, 2017
Summary: S-adenosylmethionine (SAM) is an important metabolite as a methyl-group donor in DNA and histone methylation, tuning regulation of gene expression. Appropriate intracellular SAM levels must be maintained, because methyltransferase reaction rates
Hiroki Shima   +9 more
doaj   +1 more source

Methionine regulates self-renewal, pluripotency, and cell death of GIC through cholesterol—rRNA axis

open access: yesBMC Cancer, 2022
Background Glioma-initiating cells (GICs) are the source of glioma cells that can self-renew, have pluripotency, and are treatment-resistant, so are the starting point for relapse and eventual death despite multimodality therapy.
Kiyotaka Yokogami   +6 more
doaj   +1 more source

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