Browse our Huntingtin (HTT) ELISA Kits

Full name:
Huntingtin ELISA Kits (HTT)
On www.antibodies-online.com are 23 Huntingtin (HTT) ELISA Kits from 7 different suppliers available. Additionally we are shipping Huntingtin Antibodies (158) and Huntingtin Proteins (2) and many more products for this protein. A total of 185 Huntingtin products are currently listed.
Synonyms:
AI256365, C430023I11Rik, CG9995, dhtt, Dmel\\CG9995, Hd, Hdh, Hsap\\HD, htt, huntington, IT15, SLC6A4, ZHD
list all ELISA KIts Gene Name GeneID UniProt
HTT 3064 P42858
HTT 15194 P42859
HTT 29424  

Show all species

Show all synonyms

Huntingtin (HTT) ELISA Kits by Reactivity

Select your species

More ELISA Kits for Huntingtin Interaction Partners

Zebrafish Huntingtin (HTT) interaction partners

  1. 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.

  2. the effects of Htt deficiency in early zebrafish development.

  3. In vivo, huntingtin deficient zebrafish had a severe phenotype and reduced expression of LXR (show NR1H3 ELISA Kits) reg'd genes. An LXR (show NR1H3 ELISA Kits) agonist partially rescued the phenotype and expression of LXR (show NR1H3 ELISA Kits) target genes in huntingtin deficient zebrafish during early development.

Fruit Fly (Drosophila melanogaster) Huntingtin (HTT) interaction partners

  1. Mutant HTT causes severe mislocalization and aggregation of nucleoporins and defective nucleocytoplasmic transport.

  2. Early-onset sleep defects in mutated HTT Drosophila models of Huntington's disease reflect alterations of PKA/CREB (show CREB ELISA Kits) signaling.

  3. Htt aggregates cause non-cell-autonomous pathology, including loss of vulnerable neurons that can be prevented by inhibiting endocytosis in these neurons.

  4. 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.

  5. findings support a role for HTT on dynamin 1 (show DNM1 ELISA Kits) function and ER homoeostasis. Proteolysis-induced alteration of this function may be relevant to disease.

  6. Htt modulated histone H3K9 methylation levels at the heterochromatin-euchromatin boundary.

  7. In Drosophila, Huntingtin genetically interacts with autophagy pathway components.

  8. Decreased O-linked GlcNAcylation protects from cytotoxicity mediated by huntingtin exon1 protein fragment

  9. Loss of huntingtin protein results in the disruption of Rab11 vesicle transport.

  10. The specific disruption of Drosophila huntingtin in neuroblast precursors leads to spindle misorientation; Drosophila huntingtin restores spindle misorientation in mammalian cells.

Human Huntingtin (HTT) interaction partners

  1. Although the mutant huntingtin gene is expressed widely, neurons of the striatum and cortex are selectively affected in Huntington's disease (HD). Our results suggest that this selectivity is attributable to the reduced expression of Foxp1 (show FOXP1 ELISA Kits), a protein expressed selectively in striatal and cortical neurons that plays a neuroprotective role in these cells.

  2. Huntingtin 513 fragment has unique physical interactions with the cellular environment, including, but not limited to, the protein degradation machinery.

  3. The CAG repeat (show CELF3 ELISA Kits) expansion in the exon 1 of the protein huntingtin (HTTex1) that causes the disease leads to the formation of HTT fibrils in vitro and vivo. The fibrils of mutant HTTex1 are able to seed the aggregation of wild type HTTex1 into amyloid fibrils, which in turn can seed the fibril formation of mutant HTTex1.

  4. Mutant HTT causes severe mislocalization and aggregation of nucleoporins and defective nucleocytoplasmic transport.

  5. although we were unable to detect HD-associated DNA methylation (show HELLS ELISA Kits) alterations at queried sites, we found that DNA methylation (show HELLS ELISA Kits) may be correlated to the age of disease onset in cortex tissues. Moreover, our data suggest that DNA methylation (show HELLS ELISA Kits) may, in part, contribute to tissue-specific HTT transcription through differential CTCF (show CTCF ELISA Kits) occupancy.

  6. Data, including data from studies on synthetic RNA modeling RNA repeat expansions found in patients with Huntington's disease (mRNA for exon 1 of Huntingtin protein) and myotonic dystrophy type 1 (mRNA for 3prime untranslated region of dystrophia myotonica-protein kinase (show DMPK ELISA Kits)), suggest internal loops of r(3xCAG) are stabilized by one-hydrogen bond AA pairs, while those of r(3xCUG) prefer one- or two-hydrogen bond UU pairs.

  7. This ability of huntingtin to sense ROS (show ROS1 ELISA Kits) levels at the ER, with phosphorylation and nuclear localization as a response, suggests that ROS (show ROS1 ELISA Kits) stress due to aging could be a critical molecular trigger of huntingtin functions and dysfunctions in HD and may explain the age-onset nature of the disorder.

  8. Compound heterozygous variants in HTT identified in siblings with an autosomal recessive neurodevelopmental disorder.

  9. we propose that Wig1 (show ZMAT3 ELISA Kits), a key p53 (show TP53 ELISA Kits) downstream molecule in HD condition, play an important role in stabilizing mutant Htt mRNA and thereby accelerating HD pathology in the mHtt-p53 (show TP53 ELISA Kits)-Wig1 (show ZMAT3 ELISA Kits) positive feedback manner

  10. Results suggest that the disruption of untranslated region upstream to the open reading frame (uORF) through CRISPR-Cas9 influences the translation of the mutant Huntingtin gene (mHTT) negatively and, to a lesser extent, disrupts the exon1-intron boundary, which affects the translation of the mHTT.

Mouse (Murine) Huntingtin (HTT) interaction partners

  1. Study found that Q175FDN mice exhibited earlier onset and a greater variety and severity of Huntington disease (HD)-like phenotypes as compared to Q175F mice. The characterization of Q175FDN mice suggests this model offers an improved reproduction of HD phenotypes with the mutation in the knocked-in heterozygous state.

  2. Here we show that elimination of Htt expression in the adult mouse results in behavioral deficits, progressive neuropathological changes including bilateral thalamic calcification, and altered brain iron homeostasis.

  3. Although the mutant huntingtin gene is expressed widely, neurons of the striatum and cortex are selectively affected in Huntington's disease (HD). Our results suggest that this selectivity is attributable to the reduced expression of Foxp1 (show FOXP1 ELISA Kits), a protein expressed selectively in striatal and cortical neurons that plays a neuroprotective role in these cells.

  4. Mutant huntingtin markedly accelerates compromised nuclear envelope integrity, impaired nucleocytoplasmic transport, and accumulation of DNA double-strand breaks associated with aging. HTT-linked polyQ initially accumulates in nuclei, leading to disruption of nuclear envelope architecture, partial sequestration of factors essential for nucleocytoplasmic transport (Gle1 (show GLE1 ELISA Kits) and RanGAP1 (show RANGAP1 ELISA Kits)), and intranuclear accumulation of mRNA.

  5. Mutant HTT causes severe mislocalization and aggregation of nucleoporins and defective nucleocytoplasmic transport.

  6. This ability of huntingtin to sense ROS (show ROS1 ELISA Kits) levels at the ER, with phosphorylation and nuclear localization as a response, suggests that ROS (show ROS1 ELISA Kits) stress due to aging could be a critical molecular trigger of huntingtin functions and dysfunctions in HD and may explain the age-onset nature of the disorder.

  7. HTT is required for the multipolar-bipolar transition of projection neurons and for the maintenance of their bipolar shape during their radial migration. HTT mediates these effects in vivo through the regulation of RAB11-dependent N-Cadherin trafficking. HD pathological HTT alters RAB11-dependent neuronal migration.

  8. This study found that mutant huntingtin protein (mHtt) at the endogenous level decreases BDNF (show BDNF ELISA Kits) secretion from astrocytes by disrupting the conversion of GTP (show AK3 ELISA Kits)-Rab3a (show RAB3A ELISA Kits) into GDP-Rab3a (show RAB3A ELISA Kits) and that overexpressing Rab3a (show RAB3A ELISA Kits) can rescue this deficient BDNF (show BDNF ELISA Kits) release and early neuropathology in HD knock-in mouse brain.

  9. ubiquitin binding was remarkably consistent across age groups regardless of Huntington's disease mouse model or mutant huntingtin aggregation stage even when binding of the other antibodies increased with age; it is not present in all inclusion bodies or necessary for their development

  10. N-terminal acetylation influences the aggregation of htt and its interaction with lipid bilayers

Huntingtin (HTT) Antigen Profile

Antigen Summary

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.

Alternative names and synonyms associated with Huntingtin (HTT)

  • solute carrier family 6 (neurotransmitter transporter, serotonin), member 4 (SLC6A4) Elisa Kit
  • huntingtin (LOC100216476) Elisa Kit
  • huntingtin (htt) Elisa Kit
  • huntingtin (Htt) Elisa Kit
  • huntingtin (HTT) Elisa Kit
  • huntingtin (HDH) Elisa Kit
  • AI256365 Elisa Kit
  • C430023I11Rik Elisa Kit
  • CG9995 Elisa Kit
  • dhtt Elisa Kit
  • Dmel\\CG9995 Elisa Kit
  • Hd Elisa Kit
  • Hdh Elisa Kit
  • Hsap\\HD Elisa Kit
  • htt Elisa Kit
  • huntington Elisa Kit
  • IT15 Elisa Kit
  • SLC6A4 Elisa Kit
  • ZHD Elisa Kit

Protein level used designations for Huntingtin (HTT) ELISA Kits

huntingtin , etID309952.1 , CG9995-PA , CG9995-PB , htt-PA , htt-PB , Huntington's disease protein , huntingtin (Huntington disease) , solute carrier family 6 (neurotransmitter transporter, serotonin), member 4 , Huntington disease , huntingtin-like , huntington disease protein , HD protein homolog , Huntington disease gene homolog , huntington disease protein homolog

GENE ID SPECIES
100053721 Equus caballus
100216476 Ovis aries
30214 Danio rerio
43392 Drosophila melanogaster
373520 Strongylocentrotus purpuratus
461084 Pan troglodytes
493287 Xenopus (Silurana) tropicalis
700306 Macaca mulatta
100015315 Monodelphis domestica
100145818 Ciona intestinalis
100219938 Taeniopygia guttata
100329031 Saccoglossus kowalevskii
100403524 Callithrix jacchus
100466808 Ailuropoda melanoleuca
3064 Homo sapiens
15194 Mus musculus
29424 Rattus norvegicus
479074 Canis lupus familiaris
397014 Sus scrofa
615059 Bos taurus
100351801 Oryctolagus cuniculus
422878 Gallus gallus
Selected quality suppliers for Huntingtin (HTT) ELISA Kits
Did you look for something else?