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anti-Human Huntingtin Antibodies:
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Human Polyclonal Huntingtin Primary Antibody for ELISA, ICC - ABIN4320700
Hall, Georgel: CHD proteins: a diverse family with strong ties. in Biochemistry and cell biology = Biochimie et biologie cellulaire 2007
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Human Monoclonal Huntingtin Primary Antibody for IHC (fro), IP - ABIN2474102
Moleman, Versluis, Bruinvels: Is morphine-induced catalepsy related to activation of dopaminergic neurones? in Psychopharmacology 1979
Show all 4 Pubmed References
Human Monoclonal Huntingtin Primary Antibody for ELISA, WB - ABIN516379
Thompson, Aiken, Kaltenbach, Agrawal, Illes, Khoshnan, Martinez-Vincente, Arrasate, ORourke, Khashwji, Lukacsovich, Zhu, Lau, Massey, Hayden, Zeitlin, Finkbeiner, Green, LaFerla, Bates, Huang et al.: IKK phosphorylates Huntingtin and targets it for degradation by the proteasome and lysosome. ... in The Journal of cell biology 2009
Human Monoclonal Huntingtin Primary Antibody for IHC (fro), IP - ABIN2474103
Tseng, Hsu: A kinetic analysis of the repair of radiation-induced DNA double-strand breaks. in Radiation research 1990
Show all 4 Pubmed References
These investigations demonstrate a specific 'rate-limiting' role for huntingtin in formation of the telencephalon and the pre-placodal region, and differing levels of requirement for huntingtin function in specific nerve cell types.
the effects of Htt deficiency in early zebrafish development.
In vivo, huntingtin deficient zebrafish had a severe phenotype and reduced expression of LXR (show NR1H3 Antibodies) reg'd genes. An LXR (show NR1H3 Antibodies) agonist partially rescued the phenotype and expression of LXR (show NR1H3 Antibodies) target genes in huntingtin deficient zebrafish during early development.
Data strongly suggest that mutant Htt expression exclusively in all the CNS and PNS neurons leads to fluctuation of body weight, carbohydrate and protein stores, global lipid levels along with the intracellular lipid deposits through its effect on the integrated process of metabolic homeostasis. These results also support the idea that lipid metabolism remains centrally affected in HD leading to altered body weight.
These results therefore identify native Htt as a regulator of synaptic capture and neuropeptide storage.
Mutant HTT causes severe mislocalization and aggregation of nucleoporins and defective nucleocytoplasmic transport.
Early-onset sleep defects in mutated HTT Drosophila models of Huntington's disease reflect alterations of PKA/CREB signaling.
Htt aggregates cause non-cell-autonomous pathology, including loss of vulnerable neurons that can be prevented by inhibiting endocytosis in these neurons.
Glia regulate steady-state numbers of Htt aggregates expressed in neurons through a clearance mechanism that requires the glial scavenger receptor Draper and downstream phagocytic machinery.
findings support a role for HTT on dynamin 1 (show DNM1 Antibodies) function and ER homoeostasis. Proteolysis-induced alteration of this function may be relevant to disease.
Htt modulated histone H3K9 methylation levels at the heterochromatin-euchromatin boundary.
In Drosophila, Huntingtin genetically interacts with autophagy pathway components.
Decreased O-linked GlcNAcylation protects from cytotoxicity mediated by huntingtin exon1 protein fragment
CAG repeat (show CELF3 Antibodies) length in the mutant allele was found to be a relatively consistent and significant risk factor for the progression of Huntington disease.
Study of gene expression profiles of human Huntington disease (HD) brains and HTT transgenic model rats. Results show for the first time that TFIID (show TBP Antibodies) complex formation is reduced, while soluble TBP (show TBP Antibodies) is increased in an HD model. This finding suggests that mutant HTT is a competitor instead of a recruiter of polyQ-containing transcription factors in the transcription process in HD.
Studies show that distinct protein homeostasis (proteostasis) nodes such as chaperone-mediated folding and proteolytic systems regulate the aggregation and degradation of HTT. The ability to maintain proteostasis of HTT declines during the aging process. Conversely, mechanisms that preserve proteostasis delay the onset of Huntington's disease. [review]
Studies indicate huntingtin (htt) as contributing factor to the development of Huntington's disease.
To address the function of normal HTT protein we generated HTT(+/-) and HTT(-/-) lines. The same phenotype emerged in HTT(-/-) but not HTT(+/-) lines. Conclude that Huntington disease (HD) is a developmental disorder characterized by chromosomal instability that impairs neurogenesis, and that HD represents a genetic dominant-negative loss of function, contrary to the prevalent gain-of-toxic-function hypothesis.
APP (show APP Antibodies) heterozygosity results in greater decreases of cortical APP (show APP Antibodies) in Transgenic (Tg) versus non-Tg mice. Mutant huntingtin transgenic mice develop brain iron accumulation as a result of greater suppression of APP (show APP Antibodies) levels. Elevated brain iron in Tg mice was associated with a decline in motor endurance consistent with a disease promoting effect of iron in the YAC128 model of human Huntington's Disease.
A pathogenic HTT form (polyQ-HTT) probably disrupts the protein-protein interactions in hippocampus and distorts the dynamics of molecular processes in the synapses.
Study examined the cellular and behavioural consequences of local overexpression of mutant huntingtin (mHTT) in the hippocampus of adult mice; and showed that local expression of mHTT in the dentate gyrus has deleterious effects, including its neurogenic capacity, with functional behavioural consequences, which fits well with recent data on hippocampal deficits seen in patients with Huntington's disease.
findings indicate that htt(NT) molecules do not have a strong orientational preference for parallel or antiparallel orientation of the helices within the aggregate. However, a parallel packed bundle of helices would support the idea of increased polyglutamine concentration, to pave the way for cross-beta structures.
Between July 1999 and January 2004, 1001 clinically unaffected adults at risk for HD who had chosen not to undergo predictive genetic testing for the presence or absence of the mutated HTT gene were enrolled in this non-interventional, observational, longitudinal study
Knockdown of DNMT3A (show DNMT3A Antibodies) or DNMT1 (show DNMT1 Antibodies) protected neurons against mutant Htt-induced toxicity, together demonstrating a requirement for DNMTs in mutant Htt-triggered neuronal death and suggesting a neurodegenerative mechanism based on DNA methylation (show HELLS Antibodies)-mediated transcriptional repression.
Soluble mutant Httex1 stimulated the largest changes in the Neuro2a cells tanscriptome. Inactivated CREB (show CREB1 Antibodies) signalling is the most profound impact arising from soluble Httex1.
This study demonstrates that loss of Htt function during neural development leads to HD-like neurological abnormalities in mice.
treating BACHD cortical neurons with ApiCCT1 prevented BACHD striatal neuronal atrophy by enhancing release of BDNF (show BDNF Antibodies) that subsequently acts through tyrosine receptor kinase B (TrkB (show NTRK2 Antibodies)) receptor on striatal neurons. Our findings are evidence that TRiC (show MARVELD2 Antibodies) reagent-mediated reductions in mHTT enhanced BDNF (show BDNF Antibodies) delivery to restore the trophic status of BACHD striatal neurons.
identify 4 huntingtin-targeting miRNAs viz. miR (show MLXIP Antibodies)-125b, miR (show MLXIP Antibodies)-146a, miR (show MLXIP Antibodies)-150 and miR (show MLXIP Antibodies)-214 as candidate miRNAs responsible for observed inhibitory effect of HSF1 (show HSF1 Antibodies) on huntingtin expression.
cells expressing mutant huntingtin have a dysregulated transcriptional response to epidermal growth factor (show EGF Antibodies) stimulation
Mutant htt is implicated in Huntington's disease-related alterations of neurotransmission.
The authors show that disease-inducing Huntingtin (mHtt) protein fragments display three distinct dynamic states in living cells - 1) fast diffusion, 2) dynamic clustering and 3) stable aggregation.
Study investigates the consequence of deleting mouse Huntingtin's (Htt's) N17 domain or a combination of its polyQ stretch and PRR (show PVRL1 Antibodies) (QP) on normal Htt function in mice. findings support the hypothesis that Htt's N17 and QP domains are dispensable for its critical functions during early embryonic development, but are likely more important for Htt functions in CNS development or maintenance.
Mutant Htt reduces expression of alphaB-crystallin (show CRYAB Antibodies) in astrocytes to decrease exosome secretion in Huntigton disease brains.
Huntingtin is a disease gene linked to Huntington's disease, a neurodegenerative disorder characterized by loss of striatal neurons. This is thought to be caused by an expanded, unstable trinucleotide repeat in the huntingtin gene, which translates as a polyglutamine repeat in the protein product. A fairly broad range in the number of trinucleotide repeats has been identified in normal controls, and repeat numbers in excess of 40 have been described as pathological. The huntingtin locus is large, spanning 180 kb and consisting of 67 exons. The huntingtin gene is widely expressed and is required for normal development. It is expressed as 2 alternatively polyadenylated forms displaying different relative abundance in various fetal and adult tissues. The larger transcript is approximately 13.7 kb and is expressed predominantly in adult and fetal brain whereas the smaller transcript of approximately 10.3 kb is more widely expressed. The genetic defect leading to Huntington's disease may not necessarily eliminate transcription, but may confer a new property on the mRNA or alter the function of the protein. One candidate is the huntingtin-associated protein-1, highly expressed in brain, which has increased affinity for huntingtin protein with expanded polyglutamine repeats. This gene contains an upstream open reading frame in the 5' UTR that inhibits expression of the huntingtin gene product through translational repression.
, Huntington's disease protein
, huntingtin (Huntington disease)
, solute carrier family 6 (neurotransmitter transporter, serotonin), member 4
, Huntington disease
, huntington disease protein
, HD protein homolog
, Huntington disease gene homolog
, huntington disease protein homolog