ArticleThe Journal of biological chemistry2009
Correlation of fragile histidine triad (Fhit) protein structural features with effector interactions and biological functions.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Abnormal FHIT protein expression may be correlated with poor prognosis in gastric cancer: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Pooled it
- A molecular basis of Ferredoxin Reductase (FdxR) mutations that result in mitochondriopathies.Journal of inorganic biochemistry · 2025Article
- Oncogenic stress response mechanisms as new therapeutic targets in cancer treatment: A review.Medicine · 2025Review
- The Rosetta Stone Hypothesis-Based Interaction of the Tumor Suppressor Proteins Nit1 and Fhit.Cells · 2023Article
- FHIT and C-MYC expression in cervical histology and cytology as biomarkers for detecting high-grade intraepithelial neoplasia in human papillomavirus-positive women.Cancer biomarkers : section A of Disease markers · 2020Article
- FHIT, a Novel Modifier Gene in Pulmonary Arterial Hypertension.American journal of respiratory and critical care medicine · 2019Article
- Identification of Fhit as a post-transcriptional effector of Thymidine Kinase 1 expression.Biochimica et biophysica acta. Gene regulatory mechanisms · 2017Article
- Article
- Tumor Suppressor Genes within Common Fragile Sites Are Active Players in the DNA Damage Response.PLoS genetics · 2016Review
- A Fhit-mimetic peptide suppresses annexin A4-mediated chemoresistance to paclitaxel in lung cancer cells.Oncotarget · 2016Article
- Network Analysis Identifies Mitochondrial Regulation of Epidermal Differentiation by MPZL3 and FDXR.Developmental cell · 2015Article
- The FHIT gene product: tumor suppressor and genome "caretaker".Cellular and molecular life sciences : CMLS · 2014Review
- Article
- Replicative Stress and the FHIT Gene: Roles in Tumor Suppression, Genome Stability and Prevention of Carcinogenesis.Cancers · 2014Article
- A knockdown with smoke model reveals FHIT as a repressor of Heme oxygenase 1.Cell cycle (Georgetown, Tex.) · 2014Article
- Characterization of the role of Fhit in suppression of DNA damage.Advances in biological regulation · 2013Article
- Initiation of genome instability and preneoplastic processes through loss of Fhit expression.PLoS genetics · 2012Article
- Hits, Fhits and Nits: beyond enzymatic function.Advances in enzyme regulation · 2011Review
- Fragile histidine triad protein: structure, function, and its association with tumorogenesis.Journal of cancer research and clinical oncology · 2010Review
- Nit1 and Fhit tumor suppressor activities are additive.Journal of cellular biochemistry · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
We have previously shown that Fhit tumor suppressor protein interacts with Hsp60 chaperone machinery and ferredoxin reductase (Fdxr) protein. Fhit-effector interactions are associated with a Fhit-dependent increase in Fdxr stability, followed by generation of reactive oxygen species and apoptosis induction under conditions of oxidative stress. To define Fhit structural features that affect interactions, downstream signaling, and biological outcomes, we used cancer cells expressing Fhit mutants with amino acid substitutions that alter enzymatic activity, enzyme substrate binding, or phosphorylation at tyrosine 114. Gastric cancer cell clones stably expressing mutants that do not bind substrate or cannot be phosphorylated showed decreased binding to Hsp60 and Fdxr and reduced mitochondrial localization. Expression of Fhit or mutants that bind interactor proteins results in oxidative damage and accumulation of cells in G(2)/M or sub-G(1) fractions after peroxide treatment; noninteracting mutants are defective in these biological effects. Gastric cancer clones expressing noncomplexing Fhit mutants show reduction of Fhit tumor suppressor activity, confirming that substrate binding, interaction with heat shock proteins, mitochondrial localization, and interaction with Fdxr are important for Fhit tumor suppressor function.
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Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.