ArticleProceedings of the National Academy of Sciences of the United States of America2004
Fhit is a physiological target of the protein kinase Src.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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
24 citing papers in PubMed, 70 citations in OpenAlex.
- Stage-resolved gene drivers of pancreatic ductal adenocarcinoma progression and therapeutic vulnerabilities.iScience · 2026Article
- Molecular and System-Level Characterization of MMP12 Suppression in Lung Cancer: A Combined Bioinformatics and Molecular Approach.International journal of molecular sciences · 2025Article
- Integrated analysis ofCell cycle (Georgetown, Tex.) · 2024Review
- The Rosetta Stone Hypothesis-Based Interaction of the Tumor Suppressor Proteins Nit1 and Fhit.Cells · 2023Article
- Chemical Proteomics of the Tumor Suppressor Fhit Covalently Bound to the Cofactor ApJournal of the American Chemical Society · 2022Article
- Tumor Suppressor Genes within Common Fragile Sites Are Active Players in the DNA Damage Response.PLoS genetics · 2016Review
- Association of activated Gαq to the tumor suppressor Fhit is enhanced by phospholipase Cβ.BMC cancer · 2015Article
- Comprehensive characterization of the genomic alterations in human gastric cancer.International journal of cancer · 2015Article
- Replicative Stress and the FHIT Gene: Roles in Tumor Suppression, Genome Stability and Prevention of Carcinogenesis.Cancers · 2014Article
- Activation state-dependent interaction between Gαq subunits and the Fhit tumor suppressor.Cell communication and signaling : CCS · 2013Article
- Fhit delocalizes annexin a4 from plasma membrane to cytosol and sensitizes lung cancer cells to paclitaxel.PloS one · 2013Article
- Multiple Patterns of FHIT Gene Homozygous Deletion in Egyptian Breast Cancer Patients.International journal of breast cancer · 2011Article
- Fragile histidine triad protein: structure, function, and its association with tumorogenesis.Journal of cancer research and clinical oncology · 2010Review
- Fhit regulates invasion of lung tumor cells.Oncogene · 2010Article
- Correlation of fragile histidine triad (Fhit) protein structural features with effector interactions and biological functions.The Journal of biological chemistry · 2009Article
- Fhit tumor suppressor: guardian of the preneoplastic genome.Future oncology (London, England) · 2008Review
- Genomic determinants of the efficiency of internal ribosomal entry sites of viral and cellular origin.Nucleic acids research · 2008Article
- Article
- The tumor suppressor Fhit acts as a repressor of beta-catenin transcriptional activity.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- The expression of FHIT, PCNA and EGFR in benign and malignant breast lesions.British journal of cancer · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The FHIT gene is a tumor suppressor that is frequently inactivated by genomic alterations at chromosomal region 3p14.2. In the last few years, a considerable amount of data describing inactivation of FHIT in a variety of human malignancies and demonstrating the tumor suppressor potential of Fhit have been reported. Despite the demonstration that FHIT functions as a tumor suppressor, the pathway through which Fhit induces apoptosis and inhibits growth of cancer cells is not known. Our data demonstrate that Fhit is a target of tyrosine phosphorylation by the Src protein kinase. We show that Src phosphorylates Y114 of Fhit in vitro and in vivo, providing insight into a biochemical pathway involved in Fhit signaling.
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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.