EC Number   |
General Information |
Reference |
|---|
   3.1.3.7 | evolution |
BPNT-1 is conserved in all eukaryotes, and belongs to a family of lithium-sensitive phosphatases that includes inositol monophosphatase and inositol polyphosphate-1-phosphatase |
750366 |
| 3.1.3.7 | evolution |
CysQ is part of the larger FIG superfamily of phosphatases that dephosphorylates a monosaccharide-containing substrate. The FIG superfamily is comprised of family members: fructose-1,6-bisphosphatase (FBPase), inositol-monophosphatases (IMPase)/polyphosphatases (IPPase), and the glpX-encoded variant of FBPase (Class II). Many members of this superfamily display promiscuous phosphatase activity toward various monosaccharide-containing substrates but are usually more efficient in one type, which identifies their subfamily class. Mtb CysQ can dephosphorylate myo-inositol 1-phosphate (IMP), fructose 1,6-bisphosphate (FBP), and 3'-phosphoadenosine 5'-monophosphate (PAP), but the catalytic efficiency is 1700 and 15000fold greater for PAP over FBP and IMP, respectively. The FIG superfamily enzymes have demonstrated a dependence on divalent metal ions and are most active with magnesium. The superfamily also displays sensitivity to monovalent metals, and members are most strongly inhibited by lithium (Li+) |
-, 749901 |
| 3.1.3.7 | malfunction |
cysQ knockout results in reduced levels of the sulfated glycolipid sulfolipid-1 and attenuation of cell growth |
-, 749901 |
| 3.1.3.7 | malfunction |
in glioma tissues, glycerophosphatidylcholine [PC(36:1)] is not detected and 3'-phosphoadenylate (pAp) content is significantly increased. The gene expressions of 3'-nucleotidases inositol monophosphatase (IMPAD-1) and 3'(2'),5'-bisphosphate nucleotidase 1 (BPNT-1)) are dramatically downregulated. Dramatic downregulation of IMPAD-1 and BPNT-1 are the primary cause for pAp dramatic accumulation |
752237 |
| 3.1.3.7 | malfunction |
loss of BPNT-1 in Caenorhabditis elegans results in the selective dysfunction two neurons, the bilaterally symmetric pair of ASJ chemosensory neurons. As a result, BPNT-1 mutants are defective in behaviors dependent on the ASJ neurons, such as dauer exit and pathogen avoidance. Acute treatment with lithium also causes dysfunction of the ASJ neurons. This effect is reversible, and mediated specifically through inhibition of BPNT-1. The selective effect of lithium on the nervous system is due in part to the limited expression of the cytosolic sulfotransferase SSU-1 in the ASJ neuron pair. Lithium, through inhibition of BPNT-1 in the nervous system, can cause selective toxicity to specific neurons, resulting in corresponding effects on behavior of Caenorhabditis elegans, molecular mechanism by which loss of BPNT-1 leads to dysfunction of the ASJ neuron, bpnt-1 phenotypes, overview. The specific expression of the cytosolic sulfotransferase SSU-1 in the ASJ neuron pair may contribute to the selective neuronal dysfunction caused by loss of BPNT-1 |
750366 |
| 3.1.3.7 | physiological function |
a Pde2 mutant strain displays a growth defect in the early growth phase. Mutation leads to an increase in cellular c-di-AMP and 5'-O-phosphonoadenylyl-(3'->5')-adenosine levels and increased resistance to oxacillin |
-, 751077 |
| 3.1.3.7 | physiological function |
because excess 3'-phosphoadenosine 5'-phosphate (PAP) alters the equilibrium of the sulfur pathway and inhibits sulfotransferases, PAP concentrations can affect the levels of sulfur-containing metabolites. PAP is removed by the phosphatase activity of CysQ, a 3',5'-bisphosphate nucleotidase, yielding AMP and phosphate, CysQ, a divalent cation metal-dependent phosphatase, is a major regulator of the sulfur activation pathway |
-, 749901 |
| 3.1.3.7 | physiological function |
bisphosphate 3'-nucleotidase (BPNT-1) is a lithium-sensitive phosphatase that catalyzes the breakdown of cytosolic 3'-phosphoadenosine-5'-phosphate (PAP), a byproduct of sulfation reactions utilizing the universal sulfate group donor 3'-phosphoadenosine-5'-phosphosulfate (PAPS). The daf-7 gene encodes a TGF-beta ligand that regulates diverse behaviors Caenorhabditis elegans and is transcriptionally activated in the ASJ chemosensory neuron pair upon exposure to the pathogenic bacteria Pseudomonas aeruginosa. BPNT-1 is required for the expression of daf-7 specifically in the ASJ neurons |
750366 |
| 3.1.3.7 | physiological function |
Gene expression of enzymes associated with 3'-phosphoadenylate (pAp) metabolism, pAp is a toxic by-product |
752237 |
| 3.1.3.7 | physiological function |
mice deficient for bisphosphate 3'-nucleotidase Bpnt1 do not exhibit skeletal defects but instead develop severe liver pathologies, including hypoproteinemia, hepatocellular damage, and in severe cases, frank whole body edema and death. These phenotypes are accompanied by tissue-specific elevations of the substrate 3'-phosphoadenosine 5'-phosphate, up to 50fold in liver, repressed translation, and aberrant nucleolar architecture. The phenotypes of the Bpnt1 knockout are rescued by generating a double mutant mouse deficient for both 3'-phosphoadenosine 5'-phosphate synthesis and hydrolysis, consistent with a mechanism in which 3'-phosphoadenosine 5'-phosphate accumulation is toxic to tissue function independent of sulfation |
730825 |
