|Application ||WB, IHC-P, IF, E|
|Other Accession||CAC09418, 10241694|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||75506 Da|
|Application Notes||HAP1 antibody can be used for detection of HAP1 by Western blot at 0.5 - 1 µg/mL. Antibody can also be used for immunohistochemistry starting at 2.5 µg/mL. For immunofluorescence start at 20 µg/mL.|
|Other Names||HAP1 Antibody: HLP, HAP2, HIP5, hHLP1, HLP1, Huntingtin-associated protein 1, Neuroan 1, HAP-1, huntingtin-associated protein 1|
|Reconstitution & Storage||HAP1 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.|
|Precautions||HAP1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Originally identified as neuronal protein that specifically associates with HTT/huntingtin and the binding is enhanced by an expanded polyglutamine repeat within HTT possibly affecting HAP1 interaction properties. Both HTT and HAP1 are involved in intracellular trafficking and HAP1 is proposed to link HTT to motor proteins and/or transport cargos. Seems to play a role in vesicular transport within neurons and axons such as from early endosomes to late endocytic compartments and to promote neurite outgrowth. The vesicular transport function via association with microtubule-dependent transporters can be attenuated by association with mutant HTT. Involved in the axonal transport of BDNF and its activity-dependent secretion; the function seems to involve HTT, DCTN1 and a complex with SORT1. Involved in APP trafficking and seems to faciltate APP anterograde transport and membrane insertion thereby possibly reducing processing into amyloid beta. Involved in delivery of gamma- aminobutyric acid (GABA(A)) receptors to synapses; the function is dependent on kinesin motor protein KIF5 and is disrupted by HTT with expanded polyglutamine repeat. Involved in regulation of autophagosome motility by promoting efficient retrograde axonal transport. Seems to be involved in regulation of membrane receptor recycling and degradation, and respective signal transduction, including GABA(A) receptors, tyrosine kinase receptors, EGFR, IP3 receptor and androgen receptor. Among others suggested to be involved in control of feeding behavior (involving hypothalamic GABA(A) receptors), cerebellar and brainstem development (involving AHI1 and NTRK1/TrkA), postnatal neurogenesis (involving hypothalamic NTRK2/TrkB), and ITPR1/InsP3R1-mediated Ca(2+) release (involving HTT and possibly the effect of mutant HTT). Via association with DCTN1/dynactin p150-glued and HTT/huntingtin involved in cytoplasmic retention of REST in neurons. May be involved in ciliogenesis. Involved in regulation of exocytosis. Seems to be involved in formation of cytoplasmic inclusion bodies (STBs). In case of anomalous expression of TBP, can sequester a subset of TBP into STBs; sequestration is enhanced by an expanded polyglutamine repeat within TBP. HAP1-containing STBs have been proposed to play a protective role against neurodegeneration in Huntigton disease (HD) and spinocerebellar ataxia 17 (SCA17).|
|Cellular Location||Cytoplasm. Cell projection, axon. Cytoplasm, cytoskeleton. Lysosome. Endoplasmic reticulum. Cytoplasmic vesicle, secretory vesicle, synaptic vesicle. Mitochondrion. Nucleus. Cytoplasmic vesicle, autophagosome. Note=Localizes to large nonmembrane-bound cytoplasmic bodies found in various types of neurons, called stigmoid bodies (STBs). Localization to neuronal processes and neurite tips is decreased by YWHAZ. In the nucleus localizes to nuclear rods (By similarity).|
|Tissue Location||Predominantly expressed in brain. Selectively expressed in neurons|
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abgent to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
email@example.com, and receive a free "I Love Antibodies" mug.
Provided below are standard protocols that you may find useful for product applications.
HAP1 Antibody: Huntington's disease (HD), a neurodegenerative disorder characterized by loss of striatal neurons, is caused by an expansion of a polyglutamine tract in the HD protein huntingtin. HAP1 was initially identified through a two-hybrid library screening; the binding of HAP1 to huntingtin correlated with the expansion of the polyglutamine tract. HAP1 also interacts with two cytoskeletal proteins (dynactin and pericentriolar autoantigen protein 1), suggesting that HAP1 may play a role in vesicular trafficking or organelle transport. HAP1 is also involved with the huntingtin-enhanced BDNF transport along the cellular microtubles. Attenuation of this process led to the loss of neurotrophic support and neuronal toxicity, which suggests that loss of this function might contribute to pathogenesis. Several alternatively spliced isoforms have been described for HAP1.
Borrell-Pagès M, Zala D, Humbert S, et al. Huntington's disease: from huntingtin function and dysfunction to therapeutic strategies. Cell Mol. Life Sci.2006; 63:2642-60.
Li X-J, L S-H, Sharp AH, et al. A huntingtin-associated protein enriched in brain with implications for pathology. Nature1995; 378:398-402.
Engelender S, Sharp AH, Colomer V, et al. Huntingtin-associated protein 1 (HAP1) interacts with the p150(Glued) subunit of dynactin. Hum. Molec. Genet.1997; 6:2205-12.
Gauthier LR, Charrin BC, Borrell-Pages M, et al. Huntingtin controls neurotrophic support and survival of neurons by enhancing BDNF vesicular transport along microtubules. Cell2004; 118:127-38.
If you have used an Abgent product and would like to share how it has performed, please click on the "Submit Review" button and provide the requested information. Our staff will examine and post your review and contact you if needed.
If you have any additional inquiries please email technical services at firstname.lastname@example.org.