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Human Monoclonal HBEGF Primary Antibody for ICC, IF - ABIN3201018
Prenzel, Zwick, Daub, Leserer, Abraham, Wallasch, Ullrich: EGF receptor transactivation by G-protein-coupled receptors requires metalloproteinase cleavage of proHB-EGF. in Nature 2000
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Human Monoclonal HBEGF Primary Antibody for 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. in Cancer research 2004
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Human Polyclonal HBEGF Primary Antibody for IF (p), IHC (p) - ABIN701050
Lebkuechner, Wilhelmsson, Möllerström, Pekna, Pekny: Heterogeneity of Notch signaling in astrocytes and the effects of GFAP and vimentin deficiency. in Journal of neurochemistry 2015
Human Monoclonal HBEGF Primary Antibody for FACS - ABIN4897711
Mandl, Drechsler, Jansen, Neideck, Noels, Faussner, Soehnlein, Weber, Döring: Evaluation of the BDCA2-DTR Transgenic Mouse Model in Chronic and Acute Inflammation. in PLoS ONE 2015
These results suggest that there is an EGF (show EGF Antibodies) signaling network in the zebrafish ovarian follicle, and the functionality of this network is self-regulated by its own members.
both HBEGF upregulation and apoptosis were rescued by exogenous MMP2 (show MMP2 Antibodies)
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 (show VEGF Antibodies)) and ventricular dilatation. These data suggest a potential pathophysiological mechanism that elevated HB-EGF can elicit VEGF (show VEGFA Antibodies) induction and hydrocephalus.
These results suggest that HBEGF is an important EGFR (show EGFR Antibodies) ligand in cervical cancer and that cervical cancer cells are the predominant source of HBEGF. Therefore, we propose an autocrine EGFR (show EGFR Antibodies) stimulation model in cervical carcinomas.
macrophage-secreted MMP-9 (show MMP9 Antibodies) released HB-EGF from macrophages, which increased MMP9 (show MMP9 Antibodies) 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 (show H2AFX Antibodies) foci half-life as well as USP9X (show USP9X Antibodies) expression, two features that could be linked to the observed effect on Mcl-1 (show MCL1 Antibodies).
Heparan sulfate proteoglycans and heparin derivatives further enhance HBEGF-induced differentiation by forming a complex with the epidermal growth factor receptor (show EGFR Antibodies)
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.
Serous carcinomatous component championed by expression of HB-EGF predisposes to recurrence/metastasis in stage I metastasis and recurrence in stage I uterine malignant mixed mullerian tumor.
via binding to hypoxia-responsive elements in MMP9 (show MMP9 Antibodies) gene, HIF1alpha (show HIF1A Antibodies) stimulated MMP9 (show MMP9 Antibodies) 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 (show NOTCH3 Antibodies) mouse model, we show that exogenous ADAM17 (show ADAM17 Antibodies) or HB-EGF restores cerebral arterial tone and blood flow responses, and identify upregulated voltage-dependent potassium channel (show KCNAB2 Antibodies) (KV) number in cerebral arterial myocytes as a heretofore-unrecognized downstream effector of TIMP3 (show TIMP3 Antibodies)-induced deficits.
HB-EGF stimulates Prss56 (show PRSS56 Antibodies) expression via EGFR (show EGFR Antibodies)-ERK (show EPHB2 Antibodies) 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 (show ACTG2 Antibodies) and collagen I.
These results indicate that ATX (show ENPP2 Antibodies)-lysophosphatidic acid-LPA3 (show LPAR3 Antibodies) signaling at the embryo-epithelial boundary induces decidualization via the canonical HB-EGF and COX-2 (show COX2 Antibodies) pathways.
our results suggest that shedding of HB-EGF from endothelium plays an important role in Ang II (show AGT Antibodies)-induced renal injury by linking Ang II (show AGT Antibodies)-AT1R (show AGTRAP Antibodies) with EGFR (show EGFR Antibodies) transactivation.
Results suggest that HB-EGF secreted from KRas-mutated colorectal cancer cells promotes intestinal myofibroblasts migration through ERK (show EPHB2 Antibodies) and JNK (show MAPK8 Antibodies) activation, which, in turn, could support cancer progression.
this study revealed that HB-EGF as well as HGF (show HGF Antibodies) 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