Ask about this productRelated genes to: FHIT protein
- Gene:
- FHIT NIH gene
- Name:
- fragile histidine triad
- Previous symbol:
- -
- Synonyms:
- FRA3B, AP3Aase
- Chromosome:
- 3p14.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-18
- Date modifiied:
- 2019-04-17
Related products to: FHIT protein
Related articles to: FHIT protein
- The functional head impulse test (fHIT) measures what individuals can see during high-acceleration passive head impulses, quantifying the percentage of correctly identified briefly flashed optotypes rather than inferring gaze stabilization from kinematic eye velocity. This paper traces the technological evolution of fHIT from its conceptual origins in dynamic visual acuity testing to its standardized protocol (80-ms presentation at peak head acceleration binned across 1,000-7,000°/s) and leverages clinical data to propose a new conceptual framework for functional vestibular assessment. Accumulated evidence reveals a stark dissociation between video head impulse test (vHIT) kinematic gain and fHIT functional performance, proving that the clinical bottleneck in real-world vestibular impairment is frequently the central capacity to integrate multisensory signals under visual and cognitive demands in real time. In peripheral vestibulopathies, fHIT demonstrates that functional vision depends entirely on the precise temporal clustering of covert saccades within the 80-ms optotype presentation window. In vestibular migraine, fHIT under optokinetic conflict could unmask central sensory re-weighting failures (sensory mismatch) completely missed by kinematic testing. In older people, fHIT performance-unlike vHIT gain-correlates with Tinetti Balance Scores, predicting fall risk with an odds ratio of 3.9, while dual-task studies confirm that concurrent cognitive load selectively degrades fHIT accuracy. Based on these converging dissociations, we propose a novel three-level functional framework that organizes gaze stabilization into peripheral reflex mechanics, saccadic substitution, and central sensory gating. This model establishes that the fHIT could directly probe the higher-level central integrative loop by simultaneously challenging gaze stabilization, visual discrimination, attentional allocation, and short-term memory encoding during unpredictable passive perturbations. This theoretical shift reframes abnormal functional performance alongside normal kinematic gain not as a paradox, but as an indicator of central processing or cognitive resource allocation/attention deficits, providing a new blueprint for tailoring advanced vestibular rehabilitation. - Source: PubMed
Publication date: 2026/09/03
Ramat StefanoGuerra Bruna Maria VittoriaMandalĂ Marco - To evaluate whether virtual reality-based vestibular rehabilitation (VR-VestRehab) added to home-based vestibular rehabilitation (HB-VestRehab) improves postural control, symptom severity, and psychological outcomes in vestibular migraine (VM). - Source: PubMed
Publication date: 2026/08/19
Kirazli GulceUzumcugil HaleKapusizoglu SumeyyeCinar EceOzdemir Huseyin NezihSaruhan Durmaz GulsumKaya IsaKirazli TayfunGokcay FigenCelebisoy Nese - Decapping Scavenger (DcpS) enzyme, a pyrophosphatase involved in mRNA regulation via mRNA cap degradation, has been identified as a promising oncology target in fragile histidine triad (FHIT) deficient cancers such as AML and GBM but remains underexplored in broader solid tumor indications. We have discovered a novel DcpS inhibitor, compound 17, which has a differentiated binding mode relative to known inhibitors, engaging the second nucleotide-binding domain of the mRNA cap substrate. Compound 17 possesses superior levels of potency in NSCLC A549 cell line relative to known inhibitors and demonstrates excellent selectivity against DcpS-insensitive cell lines, high levels of bioavailability in preclinical species, and mitigated hERG liabilities. Finally, compound 17 demonstrates oral dose-dependent efficacy in two solid tumor xenograft models, A253 and EBC-1, highlighting the promise of DcpS as a novel target in FHIT low/deficient solid tumors. - Source: PubMed
Scholz Spencer ODudnik Alexander SVasilopoulos AristidisJia Zhaozhong JAlbertson AnnaBrown Brian SChen LiyeLi RenheMa GaoyuanWang LongchengOkano AkinoriZhao XianruiJiang XingyuKarmel CalebBrady Patrick BLai ChunqiuDeokar HemantkumarDeAnda FelixRoy SomduttaMayekar ManasiChoi HanaLin LouisBelair David GJoshi AnandYoon Woo HyunMontano AndreaXie XiaopingNguyen HenryLi Haiyan SPan ChinDanna BenGurbani DeepakLi JingzhiKorepanova AllaLi TaoGururaja TarikereDing Rong-XianJain RinkuMartin Ruth LKohnken RebeccaRivkin Alexey - NIT1 is a tumor suppressor which functions as a metabolite repair enzyme to process deaminated glutathione (dGSH). Missense variants in NIT1 were analyzed from the COSMIC database to assess their structural and functional consequences. Of 59 missense variants identified, nine were flagged as deleterious. Homology modeling onto the NitFhit structure revealed two mechanistically distinct classes: active site mutations predicted to disrupt the conserved Glu-Lys-Cys (EKC) catalytic triad and surface mutations predicted to perturb the Nit1-Fhit interaction interface. This work provides a structural basis for understanding NIT1 loss of function in human cancer. - Source: PubMed
Publication date: 2026/07/22
Parajuli AnupPhan HungWalsh Susan - [This retracts the article DOI: 10.3892/ol.2018.9696.]. - Source: PubMed
Publication date: 2026/07/20
Xu ZhengfengWu JiajunCai PanZhou XiaoxiaoYi CunguoWang Bin