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Histamine N-methyltransferase is encoded by a single gene, called HNMT, which has been mapped to chromosome 2 in humans. [5]Three transcript variants have been identified for this gene in humans, which produce different protein isoforms [6] [5] due to alternative splicing, which allows a single gene to code for multiple proteins by including or excluding particular exons of a gene in the final ...
MTHFR is the rate-limiting enzyme in the methyl cycle, which includes the conversion of homocysteine into methionine. Defects in variants of MTHFR can therefore lead to hyperhomocysteinemia. [9] There are two common variants of MTHFR deficiency. In the more significant of the two, the individual is homozygous for the 677T polymorphism.
The modification may also occur at other sites, [4] but methylation at either of these sites can repress gene expression by either interfering with the binding of transcription factors or modifying chromatin structure to a repressive state. [5] Disease condition studies have largely fueled the effort in understanding the role of DNA methylation.
Elevated homocysteine is an independent risk factor for cardiovascular disease and inversely correlated to consumed vitamin B12/B6 and folate levels. [37] Homocysteine methylation to methionine is catalyzed by MTR, resulting in appropriate intracellular levels of methionine and tetrahydrofolate, alongside non-toxic homocysteine levels.
Methylation, as well as other epigenetic modifications, affects transcription, gene stability, and parental imprinting. [2] It directly impacts chromatin structure and can modulate gene transcription, or even completely silence or activate genes, without mutation to the gene itself.
Kidney disease usually causes a loss of kidney function to some degree and can result in kidney failure, the complete loss of kidney function. Kidney failure is known as the end-stage of kidney disease, where dialysis or a kidney transplant is the only treatment option.