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anti-Human HBEGF Antibodies:
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Human Monoclonal HBEGF Primary Antibody for ICC, IF - ABIN2451994
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 - ABIN3201018
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 signaling network in the zebrafish ovarian follicle, and the functionality of this network is self-regulated by its own members.
levels of the angiogenesis mediators endoglin, HB-EGF, BMP-9 and FGF-2 in patients with severe sepsis and septic shock; endoglin and HB-EGF could be involved in the host response of sepsis; additional studies are warrant to investigate their role as biomarker or therapeutic targets in sepsis
HB-EGF plays a pro-inflammatory role in the active skin and lung lesions of systemic sclerosis.
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
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) and ventricular dilatation. These data suggest a potential pathophysiological mechanism that elevated HB-EGF can elicit VEGF induction and hydrocephalus.
These results suggest that HBEGF is an important EGFR ligand in cervical cancer and that cervical cancer cells are the predominant source of HBEGF. Therefore, we propose an autocrine EGFR stimulation model in cervical carcinomas.
macrophage-secreted MMP-9 released HB-EGF from macrophages, which increased MMP9 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 foci half-life as well as USP9X expression, two features that could be linked to the observed effect on Mcl-1.
Heparan sulfate proteoglycans and heparin derivatives further enhance HBEGF-induced differentiation by forming a complex with the epidermal growth factor receptor
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.
Annexin A2 and HB-EGF are overexpressed and are being secreted into serum in Her-2 negative breast cancer patients.
Study demonstrates that HBEGF is post-transcriptionally regulated by low O2 (placental environment) through a mechanism involving interactions of miRNAs with its 3'UTR.
MMP14 plays an important mechanistic role in NSCLC progression, by supporting cancer invasiveness, promoting collagen degradation, and releasing HB-EGF, which accelerates lung tumor progression.
These results indicate that this new anti-HB-EGF mAb 2-108 would be useful in the diagnosis of HB-EGF-related cancers and would be a strong tool in both basic and clinical research on HB-EGF.
This antibody reacts with human HB-EGF but not mouse HB-EGF. No cross-reactivity to other EGFR ligands was observed by antigen ELISA.
HB-EGF is a molecular target for the resistance of ovarian cancer to paclitaxel and CRM197 as a HB-EGF-targeted agent might be a chemosensitizing agent for paclitaxel-resistant ovarian carcinoma
Data suggest that placental expression of HBEGF, EGF (epidermal GF), and TGFA (transforming GF alpha) is down-regulated in pre-eclampsia as compared to normal term birth; each growth factor blocks cell death/apoptosis of cytotrophoblast cell line.
Both autocrine and paracrine actions of HB-EGF play important roles in ocular angiogenesis.
via binding to hypoxia-responsive elements in MMP9 gene, HIF1alpha stimulated MMP9 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 mouse model, we show that exogenous ADAM17 or HB-EGF restores cerebral arterial tone and blood flow responses, and identify upregulated voltage-dependent potassium channel (KV) number in cerebral arterial myocytes as a heretofore-unrecognized downstream effector of TIMP3-induced deficits.
HB-EGF stimulates Prss56 expression via EGFR-ERK 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 and collagen I.
These results indicate that ATX-lysophosphatidic acid-LPA3 signaling at the embryo-epithelial boundary induces decidualization via the canonical HB-EGF and COX-2 pathways.
our results suggest that shedding of HB-EGF from endothelium plays an important role in Ang II-induced renal injury by linking Ang II-AT1R with EGFR transactivation.
Results suggest that HB-EGF secreted from KRas-mutated colorectal cancer cells promotes intestinal myofibroblasts migration through ERK and JNK activation, which, in turn, could support cancer progression.
this study revealed that HB-EGF as well as HGF 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.
Pelvic irradiation increases versican expression in bladder and rectum.
Psychiatric, social-behavioral and cognitive abnormalities were also observed in hippocampal Hbegf knockout mice.
HB-EGF promotes enteric neural stem cell proliferation and migration in a mouse model
mice in which DTR is expressed on conventional Dendritic cells display marked lymph node hypocellularity and reduced frequency of Dendritic cells in the same organs but not in spleen or nonlymphoid tissues.
miR-96 promotes osteogenic differentiation by inhibiting HB-EGF and by blocking the HB-EGF-EGFR signaling pathway in osteoblastic cells
Reverse transcriptase polymerase chain reaction studies showed that three members, Tgfa, Hbegf,and Nrg1 of the EGF family were expressed in the epithelium cultured with FGF7 + LPA as well as in the epithelium freshly isolated from the rudiments.
Decreased nitric oxide bioavailability leads to increased HB-EGF expression, which may be an important mediator of the resulting progressive diabetic nephropathy in eNOS-knockout diabetic mice.
HB-EGF changed morphology of 2D and Bioactive3D cultured astrocytes toward a radial glia-like phenotype and induced the expression of intermediate filament and progenitor cell marker protein nestin.
HB-EGF induction on Snail expression is dependent on the EGFR-ERK-Stat3 pathway.
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