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anti-Human HAP1 Antikörper:
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Human Monoclonal HAP1 Primary Antibody für ICC, FACS - ABIN259097
Chan, Nasir, Gutekunst, Coleman, Maclean, Maas, Metzler, Gertsenstein, Ross, Nagy, Hayden: Targeted disruption of Huntingtin-associated protein-1 (Hap1) results in postnatal death due to depressed feeding behavior. in Human molecular genetics 2002
Show all 7 Pubmed References
Human Polyclonal HAP1 Primary Antibody für IHC, ELISA - ABIN1002402
Borrell-Pagès, Zala, Humbert, Saudou: Huntington's disease: from huntingtin function and dysfunction to therapeutic strategies. in Cellular and molecular life sciences : CMLS 2006
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Monoclonal HAP1 Primary Antibody für IHC (fro), IP - ABIN534035
Gutekunst, Torre, Sheng, Yi, Coleman, Riedel, Bujo: Stigmoid bodies contain type I receptor proteins SorLA/LR11 and sortilin: new perspectives on their function. in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 2003
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Human Polyclonal HAP1 Primary Antibody für IHC (p), WB - ABIN541306
Engelender, Sharp, Colomer, Tokito, Lanahan, Worley, Holzbaur, Ross: Huntingtin-associated protein 1 (HAP1) interacts with the p150Glued subunit of dynactin. in Human molecular genetics 1998
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Human Polyclonal HAP1 Primary Antibody für ELISA, WB - ABIN188689
Takeshita, Fujinaga, Zhao, Yanai, Shinoda: Huntingtin-associated protein 1 (HAP1) interacts with androgen receptor (AR) and suppresses SBMA-mutant-AR-induced apoptosis. in Human molecular genetics 2006
Mouse (Murine) Polyclonal HAP1 Primary Antibody für ELISA - ABIN547921
Rong, McGuire, Fang, Sheng, Shin, Li, Li: Regulation of intracellular trafficking of huntingtin-associated protein-1 is critical for TrkA protein levels and neurite outgrowth. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2006
Rat (Rattus) Polyclonal HAP1 Primary Antibody für IHC (fro) - ABIN537847
Ma, Savas, Yu, Culver, Chao, Tanese: Huntingtin mediates dendritic transport of ?-actin mRNA in rat neurons. in Scientific reports 2012
HAP1 is differentially expressed in the human gastrointestinal tract and is down-regulated in pancreatic adenocarcinoma.
HAP1 is expressed in endocrine cells of the human gut.
data fully support that HAP1 is a GKAP, anchoring specifically to the cGMP-dependent protein kinase isoform Ibeta, and provide further evidence that also PKG spatiotemporal signaling is largely controlled by anchoring proteins
The -141 T > G polymorphism, but not the 1349 T > G polymorphism, may have protective effects for lung cancer.
HAP1 gene expression is related to the radiosensitivity of breast cancer cells and may play an important role in the regulation of cellular radiosensitivity
Overexpression of HAP1 reduced in vitro cell growth in breast cancer cell lines.
The results of this study found no association was found between the HAP1 T441M polymorphism and the age at onset of Huntington's disease .
The results of this study suggested that HAP1 co-localizes and associates with APP in physiological conditions of mouse and human brain.
WT HTT regulates ciliogenesis by interacting through huntingtin-associated protein 1 (HAP1) with pericentriolar material 1 protein (PCM1).
HAP1/stigmoid body interacts with the normal ataxin-3 through Josephin domain
sortilin stabilizes the proBDNF.HAP1 complex
ADORA2A, but not HAP1 or OGG1, may have a role in age at onset in Huntington's disease
REVIEW: function of HAP1
HAP1 may participate in axonal transport and activity-dependent release of pro-BDNF by interacting with the BDNF prodomain.
The combination of siRNA, the SB transposon, and an accurate transgenic mouse model may permit evaluation of this approach in preventing the pathogenesis associated with expression of mutant Htt.
Study provides genetic and functional evidence that the M441-HAP1 polymorphism modifies the age-at-onset of Huntington's disease .
REST/NRSF, dynactin p150(Glued), huntingtin, HAP1, and RILP form a complex involved in the translocation of REST/NRSF into the nucleus and HAP1 controls REST/NRSF cellular localization in neurons
HAP1 plays a role in the endocytosis of BDNF and its receptor in neurons.
Depleting Huntingtin-associated protein 1 (Hap1) promoted the dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A)-DDB1 and CUL4 associated factor 7 (Dcaf7) interaction and increased the DYRK1A protein level.
This study also validated the interaction between HAP1 and Sec23A using co-immunoprecipitation experiments with endogenous proteins. This manuscript also reports on the high confidence interacting partners of HAP1 identified by the non-biased approach used in this study, which interestingly, consists of predominantly trafficking-related proteins
HAP1 co-localizes with synapsin I in cortical neurons as discrete puncta
findings suggest that Hap1 is important for insulin secretion of pancreatic beta-cells via regulating the intracellular trafficking and plasma membrane localization of Cav1.2, providing new insight into the mechanisms that regulate insulin release from pancreatic beta-cells.
Early loss of Hap1 significantly reduces postnatal hippocampal neurogenesis, and leads to adult depressive-like behavior.
Hap1 interacts with Bcr on microtubules to regulate neuronal differentiation.
HAP1 regulates exocytosis by influencing the morphological docking of vesicles at the plasma membrane, the ability of vesicles to be released rapidly upon stimulation, and the early stages of fusion pore formation.
these studies identify htt and HAP1 as regulators of autophagosome transport in neurons
In the absence of HAP1, postnatal hypothalamic neurons exhibited reduced receptor tropomyosin-related kinase B (TRKB) levels.
Hap1-Tsc1 interaction regulates neuronal mTORC1 signaling and neuronal morphogenesis.
Mutant mice with Hap1 deficiency in pancreatic beta-cells had impaired glucose tolerance and decreased insulin release in response to intraperitoneally injected glucose.
Loss of Htt impaired the retrograde trafficking of PCM1 and thereby reduced primary cilia formation.
Results indicate that the Hap1-Ahi1 complex in the brainstem works as a sensor for insulin signals in feeding control.
Hap1 is critical for the transport of multiple proteins to the nerve terminals to maintain the integrity of neuronal processes
results demonstrate that HAP-1 plays an essential role in regulating postnatal feeding
HAP-1 is highly expressed in hypothalamus. Mice lacking HAP1 die after birth because of depressed feeding. The effect of mutant huntingtin on HAP1 and EGFR signaling may contribute to hypothalamic neurodegeneration and weight loss in Huntington disease
HAP1 facilitates potentiation of InsP3 receptor-1 mediated Ca2+ release.
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. This gene encodes a protein that interacts with huntingtin, with two cytoskeletal proteins (dynactin and pericentriolar autoantigen protein 1), and with a hepatocyte growth factor-regulated tyrosine kinase substrate. The interactions with cytoskeletal proteins and a kinase substrate suggest a role for this protein in vesicular trafficking or organelle transport. Several alternatively spliced transcript variants encoding different isoforms have been described for this gene.
, huntingtin-associated protein 2
, neuroan 1
, huntingtin-associated protein 1 (neuroan 1)