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These results suggest that there is an EGF (show EGF Proteins) signaling network in the zebrafish ovarian follicle, and the functionality of this network is self-regulated by its own members.
Heparan sulfate proteoglycans and heparin derivatives further enhance HBEGF-induced differentiation by forming a complex with the epidermal growth factor receptor (show EGFR Proteins)
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 (show ANXA2 Proteins) and HB-EGF are overexpressed and are being secreted into serum in Her-2 (show ERBB2 Proteins) 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 (show MMP14 Proteins) 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 (show EGFR Proteins) 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
In a clinically relevant CADASIL (show NOTCH3 Proteins) mouse model, we show that exogenous ADAM17 (show ADAM17 Proteins) or HB-EGF restores cerebral arterial tone and blood flow responses, and identify upregulated voltage-dependent potassium channel (show KCNAB2 Proteins) (KV) number in cerebral arterial myocytes as a heretofore-unrecognized downstream effector of TIMP3 (show TIMP3 Proteins)-induced deficits.
HB-EGF stimulates Prss56 expression via EGFR (show EGFR Proteins)-ERK (show EPHB2 Proteins) 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 Proteins) and collagen I.
These results indicate that ATX (show ENPP2 Proteins)-lysophosphatidic acid-LPA3 (show LPAR3 Proteins) 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 (show AGT Proteins)-induced renal injury by linking Ang II (show AGT Proteins)-AT1R (show AGTRAP Proteins) with EGFR (show EGFR Proteins) transactivation.
Results suggest that HB-EGF secreted from KRas-mutated colorectal cancer cells promotes intestinal myofibroblasts migration through ERK (show EPHB2 Proteins) and JNK (show MAPK8 Proteins) activation, which, in turn, could support cancer progression.
this study revealed that HB-EGF as well as HGF (show HGF Proteins) 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 (show Vcan Proteins) expression in bladder and rectum.
Psychiatric, social-behavioral and cognitive abnormalities were also observed in hippocampal Hbegf knockout 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