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The autosomal dominant cerebellar ataxias (ADCA) are a heterogeneous group of neurodegenerative disorders characterized by progressive degeneration of the cerebellum, brain stem and spinal cord. Additionally we are shipping Ataxin 1 Kits (25) and Ataxin 1 Proteins (8) and many more products for this protein.
Showing 10 out of 212 products:
Human Monoclonal Ataxin 1 Primary Antibody for EIA, FACS - ABIN1105458
Krishna, Mohan, Yashavantha, Rammurthy, Kiran Kumar, Mittal, Tyagi, Mukerji, Jain, Pal, Purushottam: SCA 1, SCA 2 & SCA 3/MJD mutations in ataxia syndromes in southern India. in The Indian journal of medical research 2007
Show all 4 references for ABIN1105458
Human Polyclonal Ataxin 1 Primary Antibody for EIA, WB - ABIN357975
Lim, Crespo-Barreto, Jafar-Nejad, Bowman, Richman, Hill, Orr, Zoghbi: Opposing effects of polyglutamine expansion on native protein complexes contribute to SCA1. in Nature 2008
Show all 2 references for ABIN357975
Human Polyclonal Ataxin 1 Primary Antibody for IF, WB - ABIN389309
Hong, Lee, Cho, Kang: UbcH6 interacts with and ubiquitinates the SCA1 gene product ataxin-1. in Biochemical and biophysical research communications 2008
Show all 2 references for ABIN389309
Human Polyclonal Ataxin 1 Primary Antibody for IF, ELISA - ABIN1531488
Mungall, Palmer, Sims, Edwards, Ashurst, Wilming, Jones, Horton, Hunt, Scott, Gilbert, Clamp, Bethel, Milne, Ainscough, Almeida, Ambrose, Andrews, Ashwell, Babbage, Bagguley, Bailey, Banerjee, Barker et al.: The DNA sequence and analysis of human chromosome 6. ... in Nature 2003
Ataxin-1 induces intranuclear accumulation of dAtx2/hAtaxin-2 in both Drosophila and SCA1 postmortem neurons
mutant ataxin-1 and huntingtin (show HTT Antibodies) induce developmental and late-onset neuronal pathologies in Drosophila models
SCA1 relative frequency in Poland shows the highest value compared with the data from other countries worldwide in patient with Spinocerebellar ataxias
Studied Ataxin-1 using molecular modeling to investigate the protein-protein interactions contributing to the AXH domain dimer stability.
Data indicate that in spinocerebellar ataxia (show USP14 Antibodies) type 1 patients the spinocerebellar ataxia type 1 protein trinucleotide repeat expansion (CAG)n was great than 39, comparing with normal 6-38.
This study reports the results of molecular dynamics simulations of AXH monomer of Ataxin-1.
Systematic replacement of each lysine residue in the AXH domain revealed that the lysine at 589 (K589) of ATXN1 is essential for its ubiquitylation by UbcH6 (show UBE2E1 Antibodies).
Results show that two SNPs in ATXN1 gene have a founder effect of the same repeat carrying allele as in the general Indian population suggesting that that Spinocerebellar ataxia (show USP14 Antibodies) type 1 disease onset is significantly delayed when transmission is maternal.
this work provides the structural and molecular basis of the interaction between RBM17 (show RBM17 Antibodies) and the phosphorylated form of ATXN1.
Partner recognition of the AXH domain of the transcriptional co-regulator ataxin-1 is fine-tuned by a subtle balance between self- and hetero-associations.
We measured cerebellar neurochemical alterations in a knock-in mouse model of spinocerebellar ataxia (show USP14 Antibodies) type 1, a hereditary movement disorder, using ultra-high field magnetic resonance spectroscopy (MRS).
Data indicate that the alternative ataxin-1 (ATXN1) protein is constitutively co-expressed and interacts with ATXN1.
Data establish a novel role for ATXN1 in the hippocampus as an intrinsic regulator of precursor cell proliferation, and suggest a mechanism by which polyQ expansion and loss of ATXN1 affect hippocampal function, potentially contributing to cognitive deficits and depression
The results of this study found that upregulation of cholecystokinin (Cck (show CCK Antibodies)) and subsequent interaction with the Cck1 (show CCL28 Antibodies) receptor likely underlies the lack of progressive Purkinje cell pathology in Pcp2-ATXN1[30Q]D776 mice.
Mutant ATXN1 forms oligomers whose levels correlate with disease progression in the Atxn1154Q/+ mice.
The study showed that Sca1(+)Lin(-) bone marrow contains an endodermal precursor population of cells that differentiates into hepatocytes.
HMGB1 (show HMGB1 Antibodies) facilitates repair of mitochondrial DNA damage of mutant ataxin-1 knock-in mice.
The RNA-binding protein PUMILIO1 (PUM1 (show PUM1 Antibodies)) not only directly regulates ATAXIN1 but also plays an unexpectedly important role in neuronal function. Loss of Pum1 (show PUM1 Antibodies) caused progressive motor dysfunction and SCA1-like neurodegeneration with motor impairment, primarily by increasing Ataxin1 levels.
study found a new function of ataxin-1: the modulation of Pp2a (show PPP2R2B Antibodies) activity and the regulation of its holoenzyme composition, with the polyglutamine mutation within Atxn1 altering this function in the spinocerebellar ataxia (show USP14 Antibodies) type 1 mouse cerebellum before disease onset
Delivery of either ataxin-1-like (show ATXN1L Antibodies) viral vectors to Spinocerebellar Ataxia (show USP14 Antibodies) Type 1 mice cerebella resulted in widespread cerebellar Purkinje cell transduction
downregulation of several components of the RAS-MAPK (show MAPK1 Antibodies)-MSK1 (show RPS6KA5 Antibodies) pathway decreases ATXN1 levels and suppresses neurodegeneration in mice
we show that ATXN1 reduces histone acetylation, a post-translational modification of histones associated with enhanced transcription, and represses histone acetyl transferase (show HAT1 Antibodies)-mediated transcription.
The autosomal dominant cerebellar ataxias (ADCA) are a heterogeneous group of neurodegenerative disorders characterized by progressive degeneration of the cerebellum, brain stem and spinal cord. Clinically, ADCA has been divided into three groups: ADCA types I-III. ADCAI is genetically heterogeneous, with five genetic loci, designated spinocerebellar ataxia (SCA) 1, 2, 3, 4 and 6, being assigned to five different chromosomes. ADCAII, which always presents with retinal degeneration (SCA7), and ADCAIII often referred to as the `pure' cerebellar syndrome (SCA5), are most likely homogeneous disorders. Several SCA genes have been cloned and shown to contain CAG repeats in their coding regions. ADCA is caused by the expansion of the CAG repeats, producing an elongated polyglutamine tract in the corresponding protein. The expanded repeats are variable in size and unstable, usually increasing in size when transmitted to successive generations. The function of the ataxins is not known. This locus has been mapped to chromosome 6, and it has been determined that the diseased allele contains 41-81 CAG repeats, compared to 6-39 in the normal allele, and is associated with spinocerebellar ataxia type 1 (SCA1). At least two transcript variants encoding the same protein have been found for this gene.
, spinocerebellar ataxia type 1
, spinocerebellar ataxia type 1 protein
, spinocerebellar ataxia 1 homolog
, spinocerebellar ataxia 1
, spinocerebellar ataxia type 1 protein homolog
, spinocerebellar ataxia type 1 protien