Recombinant Proteins
Product List
FHIT Human
Fragile Histidine Triad Human Recombinant
FHIT Human, GST
Fragile Histidine Triad Human Recombinant, GST Tag
The FHIT is fused to GST-Tag and purified by proprietary chromatographic techniques.
Introduction
The Fragile Histidine Triad (FHIT) is a protein encoded by the FHIT gene, located at chromosome band 3p14.2 in humans . It belongs to the histidine triad (HIT) family of nucleotide hydrolases and transferases, characterized by a conserved HxHxHxx motif . The FHIT gene spans a common fragile site (CFS) known as FRA3B, which is prone to chromosomal alterations .
Key Biological Properties: FHIT is a diadenosine 5’,5’‘’-P1,P3-triphosphate hydrolase involved in purine metabolism . It catalyzes the hydrolysis of diadenosine triphosphate (Ap3A) to AMP and ADP .
Expression Patterns: FHIT is expressed in most adult human tissues, with high expression in epithelial cells lining various organs .
Tissue Distribution: FHIT expression is notably high in the right adrenal gland, adrenal cortex, heart apex, gallbladder, oocyte, testicle, and kidney .
Primary Biological Functions: FHIT functions as a tumor suppressor, playing a crucial role in inhibiting tumor cell growth and promoting apoptosis . It also contributes to genome stability by regulating thymidine kinase 1 (TK1), an enzyme involved in thymidine triphosphate synthesis .
Role in Immune Responses and Pathogen Recognition: While FHIT’s direct role in immune responses and pathogen recognition is not well-documented, its tumor suppressor function indirectly supports immune surveillance by promoting apoptosis of damaged or cancerous cells .
Mechanisms with Other Molecules and Cells: FHIT interacts with various molecules and proteins, including binding partners involved in apoptosis and DNA damage response . It catalyzes the hydrolysis of Ap3A through a two-step mechanism .
Binding Partners and Downstream Signaling Cascades: FHIT binds to proteins such as VHL (another tumor suppressor) to enhance its tumor-suppressive effects . It also interacts with Fdxr protein in mitochondria, leading to reactive oxygen species (ROS) generation and programmed cell death .
Transcriptional Regulation: FHIT expression is regulated by promoter methylation, which can lead to gene silencing in various cancers . Loss of heterozygosity (LOH) and homozygous deletions also contribute to reduced FHIT expression .
Post-Translational Modifications: FHIT undergoes post-translational modifications that may influence its stability and activity, although specific modifications are not well-characterized .
Biomedical Research: FHIT is extensively studied for its role in cancer biology and tumor suppression . It serves as a model for understanding the mechanisms of tumor suppressor genes.
Diagnostic Tools: FHIT expression levels can be used as a biomarker for early detection of various cancers, including lung, stomach, and esophageal cancers .
Therapeutic Strategies: Gene therapy approaches using FHIT have shown promise in delaying tumor growth and inducing apoptosis in cancer cells . FHIT gene transfer has been explored as a potential treatment for pancreatic cancer .
