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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. Additionally we are shipping Huntingtin Associated Protein 1 Antibodies (68) and Huntingtin Associated Protein 1 Proteins (3) and many more products for this protein.
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Results show the stimulatory effect of PARP-1 (show PARP1 ELISA Kits) on APE1 (show APEX1 ELISA Kits)-dependent base excision repair (BER). PARP-1 (show PARP1 ELISA Kits) and APE1 (show APEX1 ELISA Kits) appear to have a functional interaction in BER since PARP-1 (show PARP1 ELISA Kits) can stimulate the strand incision activity of APE1 (show APEX1 ELISA Kits).
Early loss of Hap1 significantly reduces postnatal hippocampal neurogenesis, and leads to adult depressive-like behavior.
Hap1 interacts with Bcr (show BCR ELISA Kits) on microtubules to regulate neuronal differentiation.
increases in APEX1 (show APEX1 ELISA Kits) level confer protection against the murine paternal age effect, thus highlighting the role of APEX1 (show APEX1 ELISA Kits) in preserving reproductive health with increasing age and in protection against genotoxin-induced mutagenesis in somatic cells
Endothelial cell tumor proliferation was found to be dependent on Apex-1 (show APEX1 ELISA Kits) expression.
Expression of OGG1 (show OGG1 ELISA Kits) and APEX1 (show APEX1 ELISA Kits) was decreased at 3h after last exposure to Aroclor 1254 and only the expression level of APEX1 (show APEX1 ELISA Kits) was recovered at 24-h after, so inhibition of DNA repair can be a potential mode of action of Aroclor 1254 gonadal toxicity.
Data indicate that the endonuclease activity of APE1 is required for class switch recombination (CSR).
These results suggest that mitochondrial APE1/Ref-1 (show APEX1 ELISA Kits) is contributed to the protective role to protein kinase C (show PKC ELISA Kits)-induced mitochondrial dysfunction in endothelial cells.
Spinal motor neurones down-regulate APE1 (show APEX1 ELISA Kits) upon oxidative stress. This property renders motor neurones susceptible to continuous challenge of oxidative stress in pathological conditions.
The reductive activation of endothelial SIRT1 (show SIRT1 ELISA Kits) by APE1/Ref-1 (show APEX1 ELISA Kits) mediates the effect of APE1/Ref-1 (show APEX1 ELISA Kits) on eNOS (show NOS3 ELISA Kits) acetylation, promoting endothelium-derived NO and endothelium-dependent vasorelaxation.
data fully support that HAP1 (show APEX1 ELISA Kits) is a GKAP (show DLGAP1 ELISA Kits), anchoring specifically to the cGMP-dependent protein kinase (show CDK7 ELISA Kits) isoform Ibeta, and provide further evidence that also PKG (show PRKG1 ELISA Kits) spatiotemporal signaling is largely controlled by anchoring proteins
HAP1 (show APEX1 ELISA Kits) 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 (show APEX1 ELISA Kits) reduced in vitro cell growth in breast cancer cell lines.
The results of this study found no association was found between the HAP1 (show APEX1 ELISA Kits) T441M polymorphism and the age at onset of Huntington's disease .
The results of this study suggested that HAP1 (show APEX1 ELISA Kits) co-localizes and associates with APP (show APP ELISA Kits) in physiological conditions of mouse and human brain.
WT HTT (show HTT ELISA Kits) regulates ciliogenesis by interacting through huntingtin-associated protein 1 (HAP1) with pericentriolar material 1 protein (PCM1 (show PCM1 ELISA Kits)).
HAP1 (show APEX1 ELISA Kits)/stigmoid body interacts with the normal ataxin-3 (show ATXN3 ELISA Kits) through Josephin (show ATXN3 ELISA Kits) domain
sortilin (show SORT1 ELISA Kits) stabilizes the proBDNF.HAP1 complex
ADORA2A (show ADORA2A ELISA Kits), but not HAP1 (show APEX1 ELISA Kits) or OGG1 (show OGG1 ELISA Kits), may have a role in age at onset in Huntington's disease
REVIEW: function of HAP1 (show APEX1 ELISA Kits)
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.
AP endonuclease 1
, APEX nuclease
, DNA-(apurinic or apyrimidinic site) lyase
, apurinic-apyrimidinic endonuclease 1
, redox factor-1
, huntingtin-associated protein 2
, neuroan 1
, huntingtin-associated protein 1 (neuroan 1)