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anti-Human Ataxin 1 Antibodies:
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Human Monoclonal Ataxin 1 Primary Antibody for ELISA, FACS - ABIN968970
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
Mammalian Monoclonal Ataxin 1 Primary Antibody for ISt, IHC - ABIN1304546
Menon, Nethisinghe, Faggiano, Vannocci, Rezaei, Pemble, Sweeney, Wood, Davis, Pastore, Giunti: The role of interruptions in polyQ in the pathology of SCA1. in PLoS genetics 2013
Dog (Canine) Polyclonal Ataxin 1 Primary Antibody for ELISA - ABIN4254772
Banfi, Servadio, Chung, Kwiatkowski, McCall, Duvick, Shen, Roth, Orr, Zoghbi: Identification and characterization of the gene causing type 1 spinocerebellar ataxia. in Nature genetics 1994
This study enrolled a Chinese SCA1 pedigrees and identified 35 CAG repeats within the ATXN1 gene, which may be the shortest pathogenic allele of SCA1.
we also found that brain-region-specific differences occur early in disease initiation and progression, and they are shared across the two mouse models of SCA1. This suggests different mechanisms of degeneration at work in the inferior olive and cerebellum
These convergent evidences support ATXN1 as a promising risk gene for Schizophrenia, and the integrated approach serves as a useful tool for dissecting the genetic basis of schizophrenia.
JNK and DUSP18 reciprocally modulate the SUMOylation, which plays a regulatory role in the aggregation of ataxin-1.
ATXN1 might contribute to neuronal degeneration leading to ALS.
SCA1 mutation carriers performed similarly to controls in the postural tasks with open eyes, whereas in conditions without visual feedback SCA1 carriers had significantly higher stability index than controls at all longitudinal evaluations. Close-to-disease onset carriers (=7years) showed more prominent time-dependent stance abnormalities.
In cervical cancer cells, ATXN1 knockdown induced EMT by directly regulating Snail expression, leading to matrix metalloproteinase activation and the promotion of cell migration and invasion.
ATXN1 underexpression is associated with metabolic diseases.
data suggest GSK3b and mTOR pathways modulate this ATXN1 function in spinocerebellar ataxia type-1 (SCA1)pathogenesis that could be targeted therapeutically prior to the onset of disease symptoms in SCA1 and other pathologies involving dysregulation of ATXN1 functions.
SCA1 phenotypes could be reversed by partial suppression of human mutant ATXN1 mRNA by rAAV.miS1 when delivered after symptom onset in mice.
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 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.
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 type 1 disease onset is significantly delayed when transmission is maternal.
this work provides the structural and molecular basis of the interaction between RBM17 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 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.
expanded ATXN1 stimulates the proliferation of postnatal cerebellar stem cells in SCA1 mice. These hyperproliferating stem cells tended to differentiate into GABAergic inhibitory interneurons rather than astrocytes; this significantly increased the GABAergic inhibitory interneuron synaptic connections, disrupting cerebellar Purkinje cell function in a non-cell autonomous manner.
Reduction of protein kinase A-mediated ATXN1-pS776 results in enhanced degradation of ATXN1 and improved cerebellar-dependent motor performance.
Disruption of the ATXN1-CIC interaction shows that it is at the crux of cerebellar toxicity in spinocerebellar ataxia type 1.
Furthermore, pharmacological inhibition of PAKs decreases ATXN1 levels in a mouse model of SCA1. To explore the potential of using PAK inhibitors in combination therapy, we combined the pharmacological inhibition of PAK with MSK1, a previously identified modulator of ATXN1, and examined their effects on ATXN1 levels. We found that inhibition of both pathways results in an additive decrease in ATXN1 levels.
Sca-1(+) cardiac fibroblasts direct the type of immune cells infiltrating the heart during cardiac inflammation and drive the development of heart failure.
Functional impairment of YAP/YAPdeltaC by mutant Atxn1 during development determines the adult pathology of spinocerebellar ataxia type 1 by suppressing RORalpha-mediated transcription.
Maternal diabetes induced caspase 3-dependent apoptosis in Sca1(+) cardiac progenitor cells derived from embryonic day 17.5 (E17.5). Both maternal diabetes and high glucose in vitro activated the pro-apoptotic transcription factor, Forkhead O 3a (FoxO3a) via dephosphorylation at threonine 32 (Thr-32) residue.
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) and subsequent interaction with the Cck1 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 facilitates repair of mitochondrial DNA damage of mutant ataxin-1 knock-in mice.
The RNA-binding protein PUMILIO1 (PUM1) not only directly regulates ATAXIN1 but also plays an unexpectedly important role in neuronal function. Loss of Pum1 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 activity and the regulation of its holoenzyme composition, with the polyglutamine mutation within Atxn1 altering this function in the spinocerebellar ataxia type 1 mouse cerebellum before disease onset
Delivery of either ataxin-1-like viral vectors to Spinocerebellar Ataxia Type 1 mice cerebella resulted in widespread cerebellar Purkinje cell transduction
downregulation of several components of the RAS-MAPK-MSK1 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-mediated transcription.
Loss of ATXN1, Atxn1L and CIC is associated with hydrocephalus, omphalocele, and lung alveolarization defects.
Coiled-coil structure-dependent interactions between ataxin and Foxo lead to dendrite pathology and behavioral defects in a spinocerebellar ataxia model of Drosophila.
Ataxin-1 induces intranuclear accumulation of dAtx2/hAtaxin-2 in both Drosophila and SCA1 postmortem neurons
mutant ataxin-1 and huntingtin induce developmental and late-onset neuronal pathologies in Drosophila models
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 protein
, ataxin 1
, spinocerebellar ataxia type 1
, spinocerebellar ataxia 1 homolog
, spinocerebellar ataxia 1
, spinocerebellar ataxia type 1 protein homolog
, spinocerebellar ataxia type 1 protien