Pages that link to "Q55670781"
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The following pages link to A neurological disease caused by an expanded CAG trinucleotide repeat in the TATA-binding protein gene: a new polyglutamine disease? (Q55670781):
Displaying 50 items.
- spinocerebellar ataxia type 17 (Q21097864) (← links)
- Atrophin-1, the dentato-rubral and pallido-luysian atrophy gene product, interacts with ETO/MTG8 in the nuclear matrix and represses transcription (Q24290194) (← links)
- An autosomal dominant cerebellar ataxia linked to chromosome 16q22.1 is associated with a single-nucleotide substitution in the 5' untranslated region of the gene encoding a protein with spectrin repeat and Rho guanine-nucleotide exchange-factor dom (Q24531256) (← links)
- The SPCH1 region on human 7q31: genomic characterization of the critical interval and localization of translocations associated with speech and language disorder (Q24538769) (← links)
- Early vertebrate evolution of the TATA-binding protein, TBP (Q24645328) (← links)
- Tandem repeat copy-number variation in protein-coding regions of human genes (Q24811291) (← links)
- Spinocerebellar ataxia type 17: report of a family with reduced penetrance of an unstable Gln49 TBP allele, haplotype analysis supporting a founder effect for unstable alleles and comparative analysis of SCA17 genotypes (Q24813272) (← links)
- Precision medicine in spinocerebellar ataxias: treatment based on common mechanisms of disease (Q26764958) (← links)
- Cell biology of spinocerebellar ataxia (Q26829511) (← links)
- Mouse models of polyglutamine diseases: review and data table. Part I (Q26853025) (← links)
- Integration of modeling with experimental and clinical findings synthesizes and refines the central role of inositol 1,4,5-trisphosphate receptor 1 in spinocerebellar ataxia (Q26864714) (← links)
- Large Polyglutamine Repeats Cause Muscle Degeneration in SCA17 Mice (Q27320163) (← links)
- Interaction between mutant ataxin-1 and PQBP-1 affects transcription and cell death (Q28204152) (← links)
- The wide spectrum of spinocerebellar ataxias (SCAs) (Q28250912) (← links)
- Role of high mobility group box 1 (HMGB1) in SCA17 pathogenesis (Q28542927) (← links)
- PolyQ repeat expansions in ATXN2 associated with ALS are CAA interrupted repeats (Q28741564) (← links)
- Spinocerebellar ataxia in the Italian Spinone dog is associated with an intronic GAA repeat expansion in ITPR1 (Q30618025) (← links)
- Spinocerebellar ataxia type 17 is caused by mutations in the TATA-box binding protein (Q31127887) (← links)
- The intrinsically unstable life of DNA triplet repeats associated with human hereditary disorders (Q31497967) (← links)
- A role for voltage-dependent anion channel Vdac1 in polyglutamine-mediated neuronal cell death (Q33305438) (← links)
- Oligonucleotide-based strategies to combat polyglutamine diseases (Q33791247) (← links)
- CAG repeats determine brain atrophy in spinocerebellar ataxia 17: a VBM study (Q33818010) (← links)
- The unstable trinucleotide repeat story of major psychosis. (Q33920517) (← links)
- Transcriptional dysregulation in Huntington's disease (Q34001953) (← links)
- Exclusion of mutations in the PRNP, JPH3, TBP, ATN1, CREBBP, POU3F2 and FTL genes as a cause of disease in Portuguese patients with a Huntington-like phenotype (Q34017028) (← links)
- Role of the CCAAT-binding protein NFY in SCA17 pathogenesis (Q34243674) (← links)
- Consensus and controversies in best practices for molecular genetic testing of spinocerebellar ataxias. (Q34329735) (← links)
- Severe and rapidly progressing cognitive phenotype in a SCA17-family with only marginally expanded CAG/CAA repeats in the TATA-box binding protein gene: a case report (Q34378608) (← links)
- Indole and synthetic derivative activate chaperone expression to reduce polyQ aggregation in SCA17 neuronal cell and slice culture models. (Q34386850) (← links)
- Triplet repeats, RNA secondary structure and toxic gain-of-function models for pathogenesis (Q34446513) (← links)
- Are there CAG repeat expansion-related disorders outside the central nervous system? (Q34446570) (← links)
- PQBP-1 (Np/PQ): a polyglutamine tract-binding and nuclear inclusion-forming protein (Q34446581) (← links)
- SCA12: an unusual mutation leads to an unusual spinocerebellar ataxia (Q34446619) (← links)
- Cross linking of polyglutamine domains catalyzed by tissue transglutaminase is greatly favored with pathological-length repeats: does transglutaminase activity play a role in (CAG)(n)/Q(n)-expansion diseases? (Q34460105) (← links)
- Requirement for zebrafish ataxin-7 in differentiation of photoreceptors and cerebellar neurons (Q34505777) (← links)
- Integration of Orthogonal Signaling by the Notch and Dpp Pathways in Drosophila (Q34518118) (← links)
- Repeat associated non-ATG (RAN) translation: new starts in microsatellite expansion disorders (Q34543709) (← links)
- The Huntington's disease-like syndromes: what to consider in patients with a negative Huntington's disease gene test (Q34680311) (← links)
- Polyglutamine domain modulates the TBP-TFIIB interaction: implications for its normal function and neurodegeneration (Q34712305) (← links)
- Spinocerebellar ataxia 17 (SCA17) and Huntington's disease-like 4 (HDL4). (Q34770662) (← links)
- Population-based study of acquired cerebellar ataxia in Al-Kharga district, New Valley, Egypt (Q34879165) (← links)
- Computational neurobiology is a useful tool in translational neurology: the example of ataxia (Q34992022) (← links)
- Genetic ataxia (Q34997868) (← links)
- State of the art review: molecular diagnosis of inherited movement disorders. Movement Disorders Society task force on molecular diagnosis (Q35041284) (← links)
- Neuronal expression of TATA box-binding protein containing expanded polyglutamine in knock-in mice reduces chaperone protein response by impairing the function of nuclear factor-Y transcription factor (Q35065692) (← links)
- Proapoptotic protein glyceraldehyde-3-phosphate dehydrogenase: a possible site of action of antiapoptotic drugs (Q35092256) (← links)
- A Drosophila model of the neurodegenerative disease SCA17 reveals a role of RBP-J/Su(H) in modulating the pathological outcome (Q35155993) (← links)
- The role for alterations in neuronal activity in the pathogenesis of polyglutamine repeat disorders (Q35340099) (← links)
- Population genetics and new insight into range of CAG repeats of spinocerebellar ataxia type 3 in the Han Chinese population (Q35743563) (← links)
- The Pathogenic Role of Low Range Repeats in SCA17. (Q35743770) (← links)