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anti-Human HAX1 Antibodies:
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Human Polyclonal HAX1 Primary Antibody for ELISA, WB - ABIN449906
Chao, Parganas, Boyd, Hong, Opferman, Ihle: Hax1-mediated processing of HtrA2 by Parl allows survival of lymphocytes and neurons. in Nature 2008
data suggest that HAX-1 may be a promoting factor for AIV H9N2 replication through desensitizing PB1-F2 from its apoptotic induction in human lung epithelial cells.
the HAX1 gene is important for ovarian development, in which a p.Trp44X mutation may cause primary ovarian insufficiency in female patients
The overexpression of HAX-1 might contribute to the malignant progression of glioma.
Autophagy induction is involved in HAX1-induced cell protective mechanism, and AA127-180 serves as the functional autophagy-regulatory domain of this antiapoptotic protein.
HAX1 is a potential oncogene, and may promote the tumorigenesis and progression of hypopharyngeal carcinoma.
Oncogenic HAX-1 increases the proliferation, migration, and angiogenic activity of HUVECs. Findings provide unique insight into the pathogenesis of NPC.
Results show that Grb7 and Hax1 may colocalize partially to mitochondria in EGF-treated SKBR3 cells and their interaction can affect Caspase3 cleavage of Hax1.
results suggest that miR-223 increases the sensitivity of TNBCSCs to TRAIL-induced apoptosis by targeting HAX-1
The authors describe the first case series of patients with CN caused by HAX1 mutation who presented with HLH. They hypothesize that severe neutropenia persists after an HLH episode in children without FHLH mutations (especially infants) because these patients have CN caused by HAX1 mutations.
Study indicates that the overexpression of HAX-1 is essential in the development of chemoresistance in breast cancer.
Kv3.3 regulates Arp2/3-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 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 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 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 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 in mantle cell lymphoma.
anti-apoptotic role of HAX-1 versus BCL-XL in cytokine-dependent bone marrow-derived cells
Omi/HtrA2-HAX-1 chain played a significant role in mitochondrial homeostasis.
HAX1 plays a general role in B cell receptor-mediated internalization events and BCR-mediated apoptosis.
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 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 in skin epidermal cells stabilizes focal adhesions and impairs epidermal migration.
These findings reveal the role of HAX-1 in regulating cyclophilin-D levels via an Hsp90-dependent mechanism, resulting in protection against activation of mPTP and subsequent cell death responses.
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 and specific inhibition of IRE-1 signaling at the ER/sarcoplasmic reticulum.
Focal cerebral ischemia significantly decreased cytosolic accumulation of HAX-1, induced an upregulation of HtrA2, an upregulation of AIF and activation of caspase-3
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 muscle cells
HAX-1 represents a regulatory mechanism in cardiac calcium cycling and its responses to sympathetic stimulation, implicating its importance in calcium homeostasis and cell survival.
results indicate a different function and mechanism of Hax1 in apoptosis and re-opens the question of whether mammalian PARL, in addition to apoptosis, regulates mitochondrial stress response through Omi/HtrA2 processing.
Identification of truncated form of mouse expression of HAX-1xs and/or HAX-1s was distinctively regulated in Paneth cells of the duodenum and macrophages of the thymus after burn injury
Galpha13 stimulates cell migration through Hax-1
HAX1 is expressed in liver, kidney and testis and localised in the keratinocyte and neuronal cell line.
In functional assays, HS1-associated protein X-1 (HAX-1) expression levels influence the efficiency of B cell receptor-mediated antigen internalization.
a Bcl-2-family-related protein, Hax1, is required to suppress apoptosis in lymphocytes and neurons
tissues express three mRNA variants, encoded by two genes on chromosomes 2 and 3
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