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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 (Montrer GSK3b Kits ELISA) and mTOR (Montrer FRAP1 Kits ELISA) 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 (Montrer UBE2E1 Kits ELISA).
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.
Maternal diabetes induced caspase 3 (Montrer CASP3 Kits ELISA)-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 (Montrer FOXO3 Kits ELISA)) via dephosphorylation at threonine 32 (Thr (Montrer TRH Kits ELISA)-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 (Montrer CCK Kits ELISA)) and subsequent interaction with the Cck1 (Montrer CCL28 Kits ELISA) 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 (Montrer HMGB1 Kits ELISA) facilitates repair of mitochondrial DNA damage of mutant ataxin-1 knock-in mice.
The RNA-binding protein PUMILIO1 (PUM1 (Montrer PUM1 Kits ELISA)) not only directly regulates ATAXIN1 but also plays an unexpectedly important role in neuronal function. Loss of Pum1 (Montrer PUM1 Kits ELISA) 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
Ataxin-1 induces intranuclear accumulation of dAtx2/hAtaxin-2 in both Drosophila and SCA1 postmortem neurons
mutant ataxin-1 and huntingtin (Montrer HTT Kits ELISA) 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