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Human HAX1 Primary Antibody for SDS - ABIN1098543
Klein, Grudzien, Appaswamy, Germeshausen, Sandrock, Schäffer, Rathinam, Boztug, Schwinzer, Rezaei, Bohn, Melin, Carlsson, Fadeel, Dahl, Palmblad, Henter, Zeidler, Grimbacher, Welte: HAX1 deficiency causes autosomal recessive severe congenital neutropenia (Kostmann disease). in Nature genetics 2006
Show all 2 references for ABIN1098543
Study indicates that the overexpression of HAX-1 is essential in the development of chemoresistance in breast cancer.
Kv3.3 (show KCNC3 Proteins) regulates Arp2 (show ACTR2 Proteins)/3-dependent cortical actin nucleation mediated by Hax-1; resulting cortical actin structures interact with the channel's gating machinery to slow its inactivation rate during sustained membrane depolarizations; a mutation that leads to late-onset spinocerebellar ataxia (show USP14 Proteins) type 13.
Results show that mRNA and protein levels of HAX-1 in prostate cancer cell lines were significantly higher and inhibits cell apoptosis through caspase-9 (show CASP9 Proteins) inactivation.
HAX-1 is overexpressed in hepatocellular carcinoma and promotes cell proliferation.
HAX1 knockdown significantly decreased the proliferation. In addition, the expression levels of ki67 (show MKI67 Proteins) and phosphorylatedakt were inhibited following HAX1 knockdown.
HAX-1 was significantly elevated in laryngeal carcinoma.
Authors showed that HAX1 promotes auto-ubiquitination and degradation of cIAPs by facilitating the intermolecular homodimerization of RING finger (show PCGF1 Proteins) domain.
HAX-1 is involved in mRNA processing as an element of P-body interaction network.
HAX1 mutation is associated with severe congenital neutropenia.
HAX1 is a proto-oncogene (show RAB1A Proteins) in mantle cell lymphoma.
The hydrophilic sequences within loop 2, and the matrix-localized hydrophilic domain of UCP3, were necessary for binding to Hax-1 at the C-terminal domain, adjacent to the mitochondrial inner membrane.
Protease Omi (show HTRA2 Proteins) impairs mitochondrial function by cleaving Hax-1, which induces apoptosis in oxygen-glucose deprivation and reoxygenation -treated N2a cells and causes reperfusion injury in middle cerebral artery occlusion mice.
Knockdown of HAX1 and EB2 (show MAPRE2 Proteins) in skin epidermal cells stabilizes focal adhesions and impairs epidermal migration.
These findings reveal the role of HAX-1 in regulating cyclophilin-D (show PPIF Proteins) levels via an Hsp90 (show HSP90 Proteins)-dependent mechanism, resulting in protection against activation of mPTP (show PTPN2 Proteins) and subsequent cell death responses.
anti-apoptotic role of HAX-1 versus BCL-XL (show BCL2L1 Proteins) in cytokine-dependent bone marrow-derived cells
The expression of Hax-1 in normal brain tissue and reduction of Hax-1 in ischemic brain tissue indicate its possible involvement in pathophysiological functions in the brain.
Cardiac ischemia-reperfusion injury is associated with decreases in HAX-1 levels. Overexpression of HAX-1 promotes cardiomyocyte survival, via its interaction with Hsp90 (show HSP90 Proteins) and specific inhibition of IRE-1 (show ERN1 Proteins) signaling at the ER/sarcoplasmic reticulum.
Focal cerebral ischemia significantly decreased cytosolic accumulation of HAX-1, induced an upregulation of HtrA2 (show HTRA2 Proteins), an upregulation of AIF (show AIFM1 Proteins) and activation of caspase-3 (show CASP3 Proteins)
HAX1 deficiency: impact on lymphopoiesis and B-cell development.
HAX-1 is a multifaceted antiapoptotic protein localizing in the mitochondria and the sarcoplasmic reticulum of striated (show NSDHL Proteins) muscle cells
The protein encoded by this gene is known to associate with hematopoietic cell-specific Lyn substrate 1, a substrate of Src family tyrosine kinases. It also interacts with the product of the polycystic kidney disease 2 gene, mutations in which are associated with autosomal-dominant polycystic kidney disease, and with the F-actin-binding protein, cortactin. It was earlier thought that this gene product is mainly localized in the mitochondria, however, recent studies indicate it to be localized in the cell body. Mutations in this gene result in autosomal recessive severe congenital neutropenia, also known as Kostmann disease. Two transcript variants encoding different isoforms have been found for this gene.
HCLS1 associated protein X-1
, HCLS1-associated protein X-1
, HCLS1 (and PKD2) associated protein
, HS1 binding protein
, HS1-associating protein X-1
, HS1-binding protein 1
, HS1-associated protein X-1