Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species
Oncogenic HAX-1 increases the proliferation, migration, and angiogenic activity of HUVECs. Findings provide unique insight into the pathogenesis of NPC (show NPC1 ELISA Kits).
Results show that Grb7 (show GRB7 ELISA Kits) and Hax1 may colocalize partially to mitochondria in EGF (show EGF ELISA Kits)-treated SKBR3 cells and their interaction can affect Caspase3 cleavage of Hax1.
results suggest that miR (show MLXIP ELISA Kits)-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 (show CASP9 ELISA Kits) 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 ELISA Kits) and phosphorylatedakt were inhibited following HAX1 knockdown.
HAX-1 was significantly elevated in laryngeal carcinoma.
HAX1 plays a general role in B cell receptor-mediated internalization events and BCR (show BCR ELISA Kits)-mediated apoptosis.
The hydrophilic sequences within loop 2, and the matrix-localized hydrophilic domain of UCP3 (show UCP3 ELISA Kits), were necessary for binding to Hax-1 at the C-terminal domain, adjacent to the mitochondrial inner membrane.
Protease Omi (show HTRA2 ELISA Kits) 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 ELISA Kits) 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 ELISA Kits) levels via an Hsp90 (show HSP90 ELISA Kits)-dependent mechanism, resulting in protection against activation of mPTP (show PTPN2 ELISA Kits) and subsequent cell death responses.
anti-apoptotic role of HAX-1 versus BCL-XL (show BCL2L1 ELISA Kits) 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 ELISA Kits) and specific inhibition of IRE-1 (show ERN1 ELISA Kits) signaling at the ER/sarcoplasmic reticulum.
Focal cerebral ischemia significantly decreased cytosolic accumulation of HAX-1, induced an upregulation of HtrA2 (show HTRA2 ELISA Kits), an upregulation of AIF (show AIFM1 ELISA Kits) and activation of caspase-3 (show CASP3 ELISA Kits)
HAX1 deficiency: impact on lymphopoiesis and B-cell development.
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