A divalent cation is essential for activity. Mn2+ (2--6 mM) is most effective.
The enzyme controls intracellular levels of P1,P5-bis(5'-adenosyl)pentaphosphate and P1,P6-bis(5'-adenosyl)hexaphosphate. Weak activity with P1,P4-bis(5'-adenosyl)tetraphosphate. Marked preference for adenine over guanine nucleotides.
A divalent cation is essential for activity. Mn2+ (2--6 mM) is most effective.
The enzyme controls intracellular levels of P1,P5-bis(5'-adenosyl)pentaphosphate and P1,P6-bis(5'-adenosyl)hexaphosphate. Weak activity with P1,P4-bis(5'-adenosyl)tetraphosphate. Marked preference for adenine over guanine nucleotides.
marked preference for adenine over guanine nucleotides. The enzyme controls intracellular P1,P5-bis(5'-adenosyl)pentaphosphate and P1,P6-bis(5'-adenosyl)hexaphosphate levels
marked preference for adenine over guanine nucleotides. The most rapidly metabolised substrate appears to be P1,P5-bis(5'-adenosyl)pentaphosphate, although P1,P6-bis(5'-adenosyl)hexaphosphate is bound with higher affinity
marked preference for adenine over guanine nucleotides. The enzyme controls intracellular P1,P5-bis(5'-adenosyl)pentaphosphate and P1,P6-bis(5'-adenosyl)hexaphosphate levels
marked preference for adenine over guanine nucleotides. The most rapidly metabolised substrate appears to be P1,P5-bis(5'-adenosyl)pentaphosphate, although P1,P6-bis(5'-adenosyl)hexaphosphate is bound with higher affinity
the predominant route of P1,P6-bis(5'-adenosyl)hexaphosphate hydrolysis is to AMP plus P1,P5-bis(5'-adenosyl)pentaphosphate, with the formation of ADP plus p4A being a more minor reaction. The enzyme degrades P1,P6-bis(5'-adenosyl)hexaphosphate and P1,P5-bis(5'-adenosyl)pentaphosphate, in preference to other diadenosine polyphosphates
marked preference for adenine over guanine nucleotides. The enzyme controls intracellular P1,P5-bis(5'-adenosyl)pentaphosphate and P1,P6-bis(5'-adenosyl)hexaphosphate levels
marked preference for adenine over guanine nucleotides. The enzyme controls intracellular P1,P5-bis(5'-adenosyl)pentaphosphate and P1,P6-bis(5'-adenosyl)hexaphosphate levels
a divalent cation is essential for activity, with Mn2+ by far the most effective between 2 and 6 mM. Cu2+ supports less than 30% and Zn2+ and Co2+ each less than 3% of the maximum activity
a divalent cation is essential for activity, with Mn2+ by far the most effective between 2 and 6 mM. Cu2+ supports less than 30% and Zn2+ and Co2+ each less than 3% of the maximum activity
a divalent cation is essential for activity, with Mn2+ by far the most effective between 2 and 6 mM. Cu2+ supports less than 30% and Zn2+ and Co2+ each less than 3% of the maximum activity
a divalent cation is essential for activity, with Mn2+ by far the most effective between 2 and 6 mM. Cu2+ supports less than 30% and Zn2+ and Co2+ each less than 3% of the maximum activity
Bioinformatics Analysis Reveals an Association Between Cancer Cell Stemness, Gene Mutations, and the Immune Microenvironment in Stomach Adenocarcinoma.
no signal for hAps1 is detected in placenta, liver, skeletal muscle, kidney, spleen, colon or peripheral blood leukocytes. No activity in breast GI-101 cells, lung LX-1 cells, colon CX-1 cells, lung GI-117 cells, colon GI-112 cells and pancreas GI-103 cells
no signal for hAps1 is detected in placenta, liver, skeletal muscle, kidney, spleen, colon or peripheral blood leukocytes. No activity in breast GI-101 cells, lung LX-1 cells, colon CX-1 cells, lung GI-117 cells, colon GI-112 cells and pancreas GI-103 cells
no signal for hAps1 is detected in placenta, liver, skeletal muscle, kidney, spleen, colon or peripheral blood leukocytes. No activity in breast GI-101 cells, lung LX-1 cells, colon CX-1 cells, lung GI-117 cells, colon GI-112 cells and pancreas GI-103 cells
no signal for hAps2 is found in skeletal muscle, thymus, small intestine, colon or peripheral blood leukocytes. No activity in tumour cell lines from breast GI-101, lung LX-1, colon CX-1, lung GI-117, colon GI-112 and pancreas GI-103
no signal for hAps2 is found in skeletal muscle, thymus, small intestine, colon or peripheral blood leukocytes. No activity in tumour cell lines from breast GI-101, lung LX-1, colon CX-1, lung GI-117, colon GI-112 and pancreas GI-103
no signal for hAps2 is found in skeletal muscle, thymus, small intestine, colon or peripheral blood leukocytes. No activity in tumour cell lines from breast GI-101, lung LX-1, colon CX-1, lung GI-117, colon GI-112 and pancreas GI-103
suppressing the expression of NUDT11, SLC22A3, and HNF1B influences cellular phenotypes associated with tumor-related properties in prostate cancer cells. 4 of the 12 known risk polymorphisms are strongly associated with transcripts NUDT11, MSMB, NCOA4, SLC22A3, and HNF1B in histologically normal tissue. Although associations are also observed in tumor tissue, they tend to be more attenuated
The diadenosine hexaphosphate hydrolases from Schizosaccharomyces pombe and Saccharomyces cerevisiae are homologues of the human diphosphoinositol polyphosphate phosphohydrolase. Overlapping substrate specificities in a MutT-type protein