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anti-Human HBEGF Anticorps:
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Human Monoclonal HBEGF Primary Antibody pour ICC, IF - ABIN3201018
Prenzel, Zwick, Daub, Leserer, Abraham, Wallasch, Ullrich: EGF receptor transactivation by G-protein-coupled receptors requires metalloproteinase cleavage of proHB-EGF. dans Nature 2000
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Human Monoclonal HBEGF Primary Antibody pour ICC, IF - ABIN2451994
Miyamoto, Hirata, Yamazaki, Kageyama, Hasuwa, Mizushima, Tanaka, Yagi, Sonoda, Kai, Kanoh, Nakano, Mekada: Heparin-binding EGF-like growth factor is a promising target for ovarian cancer therapy. dans Cancer research 2004
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Human Polyclonal HBEGF Primary Antibody pour IF (p), IHC (p) - ABIN701050
Lebkuechner, Wilhelmsson, Möllerström, Pekna, Pekny: Heterogeneity of Notch signaling in astrocytes and the effects of GFAP and vimentin deficiency. dans Journal of neurochemistry 2015
Human Monoclonal HBEGF Primary Antibody pour FACS - ABIN4897711
Mandl, Drechsler, Jansen, Neideck, Noels, Faussner, Soehnlein, Weber, Döring: Evaluation of the BDCA2-DTR Transgenic Mouse Model in Chronic and Acute Inflammation. dans PLoS ONE 2015
These results suggest that there is an EGF (Montrer EGF Anticorps) signaling network in the zebrafish ovarian follicle, and the functionality of this network is self-regulated by its own members.
HB-EGF expression in serum may be a potential therapeutic indicator for novel HB-EGF-targeted therapy in recurrent ovarian cancer.
both HBEGF upregulation and apoptosis were rescued by exogenous MMP2 (Montrer MMP2 Anticorps)
Results support the idea that excess heparin binding epidermal growth factor-like growth factor (HB-EGF) leads to a significant elevation of vascular endothelial growth factor (VEGF (Montrer VEGF Anticorps)) and ventricular dilatation. These data suggest a potential pathophysiological mechanism that elevated HB-EGF can elicit VEGF (Montrer VEGFA Anticorps) induction and hydrocephalus.
These results suggest that HBEGF is an important EGFR (Montrer EGFR Anticorps) ligand in cervical cancer and that cervical cancer cells are the predominant source of HBEGF. Therefore, we propose an autocrine EGFR (Montrer EGFR Anticorps) stimulation model in cervical carcinomas.
macrophage-secreted MMP-9 (Montrer MMP9 Anticorps) released HB-EGF from macrophages, which increased MMP9 (Montrer MMP9 Anticorps) in OVCA433, resulting in a positive feedback loop to drive HB-EGF release and increase proliferation in co-culture.
Genome-wide significant (GWS) associations in single-nucleotide polymorphism (SNP)-based tests (P < 5 x 10(-8)) were identified for SNPs in PFDN1/HBEGF, USP6NL/ECHDC3, and BZRAP1-AS1.
HB-EGF is implicated in DNA double strand breaks repair as silencing of HB-EGF increased gammaH2AX (Montrer H2AFX Anticorps) foci half-life as well as USP9X (Montrer USP9X Anticorps) expression, two features that could be linked to the observed effect on Mcl-1 (Montrer MCL1 Anticorps).
Heparan sulfate proteoglycans and heparin derivatives further enhance HBEGF-induced differentiation by forming a complex with the epidermal growth factor receptor (Montrer EGFR Anticorps)
this study suggests that HBEGF promotes the formation of gliomas, is necessary for tumor maintenance and therefore may be a novel therapeutic target.
Results show that HBEGF is highly expressed in primary ovarian tumors and increases as the disease progresses.
via binding to hypoxia-responsive elements in MMP9 (Montrer MMP9 Anticorps) gene, HIF1alpha (Montrer HIF1A Anticorps) stimulated MMP9 (Montrer MMP9 Anticorps) expression, and therefore appeared as a prominent intermediary in HB-EGF-induced blood-brain barrier damage
Using the best available methods for preclinical evaluation in animal models, it is likely that HB-EGF-like growth factor treatment leads to regeneration of chronic tympanic membrane perforations and restoration of the tympanic membrane to normal function, suggesting a potential route for nonsurgical treatment.
In a clinically relevant CADASIL (Montrer NOTCH3 Anticorps) mouse model, we show that exogenous ADAM17 (Montrer ADAM17 Anticorps) or HB-EGF restores cerebral arterial tone and blood flow responses, and identify upregulated voltage-dependent potassium channel (Montrer KCNAB2 Anticorps) (KV) number in cerebral arterial myocytes as a heretofore-unrecognized downstream effector of TIMP3 (Montrer TIMP3 Anticorps)-induced deficits.
HB-EGF stimulates Prss56 (Montrer PRSS56 Anticorps) expression via EGFR (Montrer EGFR Anticorps)-ERK (Montrer EPHB2 Anticorps) pathway.
HB-EGF Tg mice were shown to develop more severe liver fibrosis when treated with carbon tetrachloride or bile duct ligation, with increased matrix metalloproteinases 13 activity and enhanced expression of fibrogenic genes including alpha-smooth muscle actin (Montrer ACTG2 Anticorps) and collagen I.
These results indicate that ATX (Montrer ENPP2 Anticorps)-lysophosphatidic acid-LPA3 (Montrer LPAR3 Anticorps) signaling at the embryo-epithelial boundary induces decidualization via the canonical HB-EGF and COX-2 (Montrer COX2 Anticorps) pathways.
our results suggest that shedding of HB-EGF from endothelium plays an important role in Ang II (Montrer AGT Anticorps)-induced renal injury by linking Ang II (Montrer AGT Anticorps)-AT1R (Montrer AGTRAP Anticorps) with EGFR (Montrer EGFR Anticorps) transactivation.
Results suggest that HB-EGF secreted from KRas-mutated colorectal cancer cells promotes intestinal myofibroblasts migration through ERK (Montrer EPHB2 Anticorps) and JNK (Montrer MAPK8 Anticorps) activation, which, in turn, could support cancer progression.
this study revealed that HB-EGF as well as HGF (Montrer HGF Anticorps) inhibited BDL-induced cholestatic liver injury by predominantly exerting acute cytoprotective and chronic antifibrotic effects, respectively.
Abnormal keratinocyte migration and down-regulated expression of the Hbegf gene might be associated with impaired eyelid development in B6-Co mice.
These results indicate that HB-EGF and its receptors expression changed in bovine endometrium throughout the oestrous cycle; IFN-tau increased their expression in cultured endometrial cells.
Heparin-binding EGF-like growth factor is main component in chromaffin granules responsible for neurotrophic effect on dopaminergic neurones. Protective effects on nigrostriatal dopaminergic neurones. Candidate for treatment of Parkinson's disease.
Growth factor that mediates its effects via EGFR, ERBB2 and ERBB4. Required for normal cardiac valve formation and normal heart function. Promotes smooth muscle cell proliferation. May be involved in macrophage-mediated cellular proliferation. It is mitogenic for fibroblasts, but not endothelial cells. It is able to bind EGF receptor/EGFR with higher affinity than EGF itself and is a far more potent mitogen for smooth muscle cells than EGF. Also acts as a diphtheria toxin receptor.
proheparin-binding EGF-like growth factor
, heparin-binding EGF-like growth factor
, Heparin-binding EGF-like growth factor
, diphtheria toxin receptor (heparin-binding EGF-like growth factor)
, diphtheria toxin receptor (heparin-binding epidermal growth factor-like growth factor)
, heparin-binding epidermal growth factor
, Diphtheria toxin receptor (heparin binding epidermal growth factor - like growth factor)
, heparin binding epidermal growth factor-like growth factor
, heparin-binding epidermal -growth - like growth factor
, heparin-binding epidermal -growth factor
, diphtheria toxin receptor
, heparin-binding epidermal growth factor-like growth factor