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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
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 (show RAB1A Antibodies), 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 (show NPC1 Antibodies).
Results show that Grb7 (show GRB7 Antibodies) and Hax1 may colocalize partially to mitochondria in EGF (show EGF Antibodies)-treated SKBR3 cells and their interaction can affect Caspase3 cleavage of Hax1.
results suggest that miR (show MLXIP Antibodies)-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 Antibodies) inactivation.
Omi/HtrA2 (show HTRA2 Antibodies)-HAX-1 chain played a significant role in mitochondrial homeostasis.
HAX1 plays a general role in B cell receptor-mediated internalization events and BCR (show BCR Antibodies)-mediated apoptosis.
The hydrophilic sequences within loop 2, and the matrix-localized hydrophilic domain of UCP3 (show UCP3 Antibodies), were necessary for binding to Hax-1 at the C-terminal domain, adjacent to the mitochondrial inner membrane.
Protease Omi (show HTRA2 Antibodies) 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 Antibodies) 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 Antibodies) levels via an Hsp90 (show HSP90 Antibodies)-dependent mechanism, resulting in protection against activation of mPTP (show PTPN2 Antibodies) and subsequent cell death responses.
anti-apoptotic role of HAX-1 versus BCL-XL (show BCL2L1 Antibodies) 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 Antibodies) and specific inhibition of IRE-1 (show ERN1 Antibodies) signaling at the ER/sarcoplasmic reticulum.
Focal cerebral ischemia significantly decreased cytosolic accumulation of HAX-1, induced an upregulation of HtrA2 (show HTRA2 Antibodies), an upregulation of AIF (show AIFM1 Antibodies) and activation of caspase-3 (show CASP3 Antibodies)
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