|Application ||IHC-P, E|
|Calculated MW||16858 Da|
|Dilution||ELISA, IHC-P (1:50 - 1:33)|
|Other Names||FHIT, AP3Aase, Dinucleosidetriphosphatase, Fragile histidine triad, Fragile histidine triad gene, AP3A hydrolase, Bis(5-adenosyl)-triphosphatase, FRA3B, Tumor suppressor protein|
|Target/Specificity||FHIT Antibody detects endogenous levels of FHIT.|
|Reconstitution & Storage||Immunoaffinity purified|
|Precautions||Anti-FHIT Antibody (aa80-129) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Cleaves P(1)-P(3)-bis(5'-adenosyl) triphosphate (Ap3A) to yield AMP and ADP. Can also hydrolyze P(1)-P(4)-bis(5'- adenosyl) tetraphosphate (Ap4A), but has extremely low activity with ATP. Modulates transcriptional activation by CTNNB1 and thereby contributes to regulate the expression of genes essential for cell proliferation and survival, such as CCND1 and BIRC5. Plays a role in the induction of apoptosis via SRC and AKT1 signaling pathways. Inhibits MDM2-mediated proteasomal degradation of p53/TP53 and thereby plays a role in p53/TP53-mediated apoptosis. Induction of apoptosis depends on the ability of FHIT to bind P(1)-P(3)-bis(5'-adenosyl) triphosphate or related compounds, but does not require its catalytic activity, it may in part come from the mitochondrial form, which sensitizes the low- affinity Ca(2+) transporters, enhancing mitochondrial calcium uptake. Functions as tumor suppressor.|
|Cellular Location||Cytoplasm. Mitochondrion. Nucleus.|
|Tissue Location||Low levels expressed in all tissues tested. Phospho-FHIT observed in liver and kidney, but not in brain and lung. Phospho-FHIT undetected in all tested human tumor cell lines|
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