The FHIT Polyclonal Antibody (PAC035190) is a valuable tool for researchers studying the FHIT protein, a tumor suppressor involved in DNA damage repair and cell cycle regulation. This antibody, produced in rabbits, exhibits high reactivity with human samples and is suitable for use in Western blotting applications. By binding to the FHIT protein, this antibody allows for the accurate detection and analysis of FHIT expression in a variety of cell types, making it an essential component of studies in oncology and molecular biology.FHIT is known for its role in maintaining genomic stability and preventing the development of cancerous cells.
Dysfunction of FHIT has been linked to various cancers, making it a promising target for anti-cancer therapies. By gaining insights into the function of FHIT, researchers can potentially uncover new strategies for treating cancer and improving patient outcomes.In conclusion, the FHIT Polyclonal Antibody is a reliable tool for investigators seeking to better understand the role of FHIT in cancer development and progression. Its specificity and sensitivity make it an indispensable resource for research aimed at elucidating the molecular mechanisms underlying tumorigenesis and identifying novel therapeutic targets for cancer treatment.
Antibody Name:
Fhit Antibody (PACO35190)
Antibody SKU:
PACO35190
Size:
50ug
Host Species:
Rabbit
Tested Applications:
ELISA
Recommended Dilutions:
Species Reactivity:
Mouse
Immunogen:
Recombinant Mouse Bis(5'-adenosyl)-triphosphatase protein (2-150AA)
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 (By similarity). Functions as tumor suppressor.
FHIT: a member of the histidine triad gene family. A diadenosine 5',5'''-P1,P3-triphosphate hydrolase involved in purine metabolism. Its gene encompasses the common fragile site FRA3B on chromosome 3, where carcinogen-induced damage can lead to translocations and aberrant transcripts of this gene. A possible tumor suppressor in specific tissues. Phospho-FHIT observed in liver and kidney, but not in brain and lung. Phospho-FHIT undetected in all tested human tumor cell lines. Aberrant transcripts from this gene have been found in about half of all esophageal, stomach, and colon carcinomas.Protein type: Motility/polarity/chemotaxis; Tumor suppressor; Hydrolase; DNA replication; EC 3.6.1.29; Nucleotide Metabolism - purineCellular Component: cytoplasm; cytosol; intracellular; nucleus; plasma membraneMolecular Function: bis(5'-adenosyl)-triphosphatase activity; catalytic activity; hydrolase activity; identical protein binding; nickel ion binding; nucleotide binding; ubiquitin protein ligase bindingBiological Process: apoptosis; diadenosine triphosphate catabolic process; DNA replication; negative regulation of proteasomal ubiquitin-dependent protein catabolic process; nucleotide metabolic process; purine nucleotide metabolic process; regulation of transcription, DNA-dependent; transcription, DNA-dependent
UniProt Protein Details:
NCBI Summary:
This gene encodes a member of the HIT family of proteins that are characterized by the presence of a histidine triad sequence. The encoded protein is a diadenosine triphosphate hydrolase enzyme that cleaves the P(1)-P(3)-bis(5'-adenosyl) triphosphate (Ap3A) to yield AMP and ADP. This locus is very fragile and has been found to be altered in different types of cancers. Mice lacking the encoded protein display increased susceptibility to spontaneous and induced tumors. Ectopic expression of the encoded protein in such knockout mice inhibits tumor development. Alternative splicing results in multiple transcript variants encoding different isoforms. [provided by RefSeq, Apr 2015]
