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S-adenosylhomocysteine hydrolase belongs to the adenosylhomocysteinase family. Additionally we are shipping AHCY Antibodies (98) and AHCY Proteins (95) and many more products for this protein.
Showing 7 out of 19 products:
SAH (show ACSM3 ELISA Kits) hydrolase deficiency can remain asymptomatic in childhood, and the disorder can be associated with early onset hepatocellular carcinoma.
H19 (show NCKAP1 ELISA Kits) knockdown activates SAHH, leading to increased DNMT3B (show DNMT3B ELISA Kits)-mediated methylation of an lncRNA-encoding gene Nctc1 within the Igf2-H19 (show NCKAP1 ELISA Kits)-Nctc1 locus.
S-adenosylhomocysteine hydrolase is regulated by lysine acetylation
SAHH can promote apoptosis, inhibit migration and adhesion of ESCC cells suggesting that it may be involved in carcinogenesis of the esophagus.
A fluorescence-based assay for the measurement of S-adenosylhomocysteine hydrolase activity in biological samples.
Maintenance of ionizable active-site residues in catalytically suitable protonation states in closed forms of placental AHCY may be assisted by a water chain, stabilized by Asp182, that can import and export protons from and to the environment.
SAHH, which is diffuse in the cytoplasm of nonmotile Dictyostelium amoebae and human neutrophils, concentrates with F-actin in pseudopods at the front of motile, chemotaxing cells
In the case of Hs-SAHH, the slow-binding phase terminates in micromolar affinity, but over a period of hours, the dissociation rate constant decreases until the final equilibrium affinity is in the nanomolar range.
We found clinically relevant levels of Hcy (0-500 microM) induced elevation of SAH (show ACSM3 ELISA Kits), declination of SAM (show TTN ELISA Kits) and SAM (show TTN ELISA Kits)/SAH (show ACSM3 ELISA Kits) ratio and reduced expression of SAHH and MBD2 (show DPEP2 ELISA Kits), but increased activity of DNMT3a (show DNMT3A ELISA Kits) and DNMT3b (show DNMT3B ELISA Kits) affecting DNA methylation (show HELLS ELISA Kits)
consider changes in charge and the sterical incompatibility in mutant p.A89V protein as main reason for enzyme malfunction with AdoHcyase deficiency as consequence
Ahcy was identified from coupling of methylation with gene expression data, shed light on the underlying mechanisms of cytosine demethylation under methyl-deficient conditions.
report the crystallization of mouse SAHH in the presence of the reaction product adenosine. The crystals diffracted to at least 1.55 A degrees resolution and are suitable for X-ray structure analysis at high resolution.
report that Myc (show MYC ELISA Kits) promotes upregulation of S-adenosyl homocysteine hydrolase.
AHCYL1 (show AHCYL1 ELISA Kits) has a different function from AHCY and plays an important role in embryogenesis by modulating inositol 1,4,5-trisphosphate receptor function for the intracellular calcium release
Hepatic steatosis and liver degeneration are prominent features of the ducttrip (dtp) mutant phenotype. Positional cloning identified a causative mutation in the gene encoding S-adenosylhomocysteine hydrolase (Ahcy).
S-adenosylhomocysteine hydrolase belongs to the adenosylhomocysteinase family. It catalyzes the reversible hydrolysis of S-adenosylhomocysteine (AdoHcy) to adenosine (Ado) and L-homocysteine (Hcy). Thus, it regulates the intracellular S-adenosylhomocysteine (SAH) concentration thought to be important for transmethylation reactions. Deficiency in this protein is one of the different causes of hypermethioninemia. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
, S-adenosyl-L-homocysteine hydrolase
, S-adenosyl-L-homocysteine hydrolase B
, adenosylhomocysteinase B
, adoHcyase B
, liver copper-binding protein