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anti-Human HAX1 Antikörper:
anti-Rat (Rattus) HAX1 Antikörper:
anti-Mouse (Murine) HAX1 Antikörper:
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Human Monoclonal HAX1 Primary Antibody für IF, IP - ABIN968199
Suzuki, Demoliere, Kitamura, Takeshita, Deuschle, Watanabe: HAX-1, a novel intracellular protein, localized on mitochondria, directly associates with HS1, a substrate of Src family tyrosine kinases. in Journal of immunology (Baltimore, Md. : 1950) 1997
Human Polyclonal HAX1 Primary Antibody für 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
Oncogenic HAX-1 increases the proliferation, migration, and angiogenic activity of HUVECs. Findings provide unique insight into the pathogenesis of NPC (zeige NPC1 Antikörper).
Results show that Grb7 (zeige GRB7 Antikörper) and Hax1 may colocalize partially to mitochondria in EGF (zeige EGF Antikörper)-treated SKBR3 cells and their interaction can affect Caspase3 cleavage of Hax1.
results suggest that miR (zeige MLXIP Antikörper)-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 (zeige CASP9 Antikörper) 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 (zeige MKI67 Antikörper) and phosphorylatedakt were inhibited following HAX1 knockdown.
HAX-1 was significantly elevated in laryngeal carcinoma.
Omi/HtrA2 (zeige HTRA2 Antikörper)-HAX-1 chain played a significant role in mitochondrial homeostasis.
HAX1 plays a general role in B cell receptor-mediated internalization events and BCR (zeige BCR Antikörper)-mediated apoptosis.
The hydrophilic sequences within loop 2, and the matrix-localized hydrophilic domain of UCP3 (zeige UCP3 Antikörper), were necessary for binding to Hax-1 at the C-terminal domain, adjacent to the mitochondrial inner membrane.
Protease Omi (zeige HTRA2 Antikörper) 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 (zeige MAPRE2 Antikörper) in skin epidermal cells stabilizes focal adhesions and impairs epidermal migration.
These findings reveal the role of HAX-1 in regulating cyclophilin-D (zeige PPIF Antikörper) levels via an Hsp90 (zeige HSP90 Antikörper)-dependent mechanism, resulting in protection against activation of mPTP (zeige PTPN2 Antikörper) and subsequent cell death responses.
anti-apoptotic role of HAX-1 versus BCL-XL (zeige BCL2L1 Antikörper) 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 (zeige HSP90 Antikörper) and specific inhibition of IRE-1 (zeige ERN1 Antikörper) signaling at the ER/sarcoplasmic reticulum.
Focal cerebral ischemia significantly decreased cytosolic accumulation of HAX-1, induced an upregulation of HtrA2 (zeige HTRA2 Antikörper), an upregulation of AIF (zeige AIFM1 Antikörper) and activation of caspase-3 (zeige CASP3 Antikörper)
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