FHIT Antibody
- Known as:
- FHIT Antibody
- Catalog number:
- 32220
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- FHIT Antibody
Related genes to: FHIT Antibody
- 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 Antibody
Related articles to: FHIT Antibody
- BackgroundMotion sickness (MS) is an autonomic condition triggered by real or perceived movement. No single objective test reliably identifies MS susceptibility or explains its vestibular basis.ObjectiveTo compare vHIT, SHIMP, and functional head impulse test (fHIT)-with and without optokinetic stimulation-in detecting vestibulo-ocular reflex (VOR) dysfunction in MS, and to examine links between MS susceptibility, dizziness-related handicap, and anxiety.MethodsThirty adults with MS and 30 healthy controls underwent vHIT, SHIMP, fHIT, and optokinetic fHIT (fHIT-OPK), along with the Motion Sickness Susceptibility Questionnaire-Short Form (MSSQ-SF), Dizziness Handicap Inventory (DHI), and State-Trait Anxiety Inventory (STAI).ResultsVOR gain did not differ significantly between groups on vHIT or SHIMP. fHIT percentage of correct answer (CA%) were significantly lower in the MS group for the right anterior ( = 0.049), left anterior ( = 0.001), and right posterior ( = 0.015) canals. fHIT-OPK revealed additional impairment in the right lateral canal ( = 0.031). DHI and STAI scores were significantly elevated in the MS group. MSSQ-SF correlated strongly with DHI total (r = 0.914) and moderately with state and trait anxiety (r = 0.541 and 0.551, respectively).ConclusionsfHIT is more sensitive than vHIT and SHIMP in detecting VOR-related dysfunction in MS. Optokinetic stimulation unmasks visual-vestibular integration deficits. Subjective measures of handicap and anxiety should complement objective testing in this population. - Source: PubMed
Publication date: 2026/09/22
Bilgili KubranurKirazli GulceOgut Mehmet Fatih - 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 VittoriaMandalà 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