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Validated All-in-One™ qPCR Primer for HBEGF(NM_001945.2) Search again
Product ID:
HQP004493
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
DTR, DTS, DTSF, HEGFL
Gene Description:
heparin binding EGF like growth factor
Target Gene Accession:
NM_001945.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Gene References into function
- Heparin-binding EGF-like growth factor decreases inducible nitric oxide synthase and nitric oxide production after intestinal ischemia/reperfusion injury.
- Site-directed mutagenesis of heparin-binding EGF-like growth factor (HB-EGF): analysis of O-glycosylation sites and properties
- HB-EGF mRNA and protein levels in gastric cancers were elevated, compared with normal gastric tissues, especially in the intestinal type.
- The current study reveals that HB-EGF mRNA is abundantly expressed in human and mouse adipose tissue, plasma HB-EGF levels increase in parallel with fat accumulation in human, and subjects with coronary artery disease have higher plasma HB-EGF levels.
- Bronchial epithelial compression regulates MAP kinase signaling and HB-EGF-like growth factor expression.
- Heparin-binding EGF-like growth factor mediates the biological effects of P450 arachidonate epoxygenase metabolites in epithelial cells
- nardilysin (NRDc) is potently inhibited by heparin-binding epidermal growth factor-like growth factor (HB-EGF)
- Helicobacter pylori-stimulated EGF receptor transactivation requires metalloprotease cleavage of HB-EGF
- data suggest that uterine receptivity may be regulated in part by the stromal-derived HB-EGF
- HB-EGF cytoprotection is due, in part, to its ability to decrease reactive oxygen species production
- Review. The mode of activation of EGFR in response to bacterial lipoteichoic acid involves cleavage of the transmembrane ligand HBEGF by ADAM 10.
- Transgenic expression of HB-EGF accelerates the proliferation of hepatocytes after partial hepatectomy
- the effect of N- and C-terminal residues of the EGF-like domain of HB-EGF in the binding affinity to the EGF receptor on A431 cells
- Diffusely expressed throughout normal and psoriatic epidermis and sparsely colocalized with EGFr in all viable epidermal layers, with increased colocalization in psoriatic epidermis.
- HB-EGF has an important role in the early pathogenesis of psoriasis.
- HB-EGF and FGF-2 act in concert to regulate the synthesis of elastin in injury/repair situations in pulmonary fibroblasts.
- proHB-EGF shedding induced by TPA and angiotensin II requires PACSIN3 as an upregulator
- Heparin-binding EGF-like growth factor has a role in Angiopoietin-mediated recruitment of vascular smooth muscle cells.
- GnRH-induced transactivation of the EGF-R and the subsequent ERK1/2 phosphorylation result from ectodomain shedding of HBEGF.
- HB-EGF blocks cytokine-induced NF-kappaB activation and decreases nitric oxide production, interferes with cytokine-induced IkappaB kinase activity, inhibits phosphorylation and degradation of IkappaBalpha, and suppresses release of proinflammatory IL-8.
- Results suggest that epidermal growth factor receptor HER-mediated autocrine and paracrine signaling by heparin-binding EGF-like growth factor or other EGF family members induces cytotrophoblast differentiation to an invasive phenotype.
- Cis-acting element mediating gastrin responsiveness was mapped to the -69 to -58 region of the HB-EGF promoter. Gastrin stimulation was PKC dependent and at least partially mediated by activation of the EGF receptor.
- The spatial and temporal pattern of HB-EGF expression suggest that HB-EGF may an important local regulator of ovarian function and structure.
- relevance of a p38-ADAM-HB-EGF-EGFR-dependent pathway and its potential significance for tumor cells in evasion of chemotherapeutic agent-induced apoptosis
- HB-EGF might be a more important tumor growth regulator of malignant fibrous histiocytoma through autocrine or paracrine pathways, when compared with betacellulin.
- HB-EGF is a potent inducer of tumor growth and angiogenesis
- the heparin-binding domain serves as a negative regulator of heparin-binding EGF-like Growth Factor
- Results indicate that pro-heparin-binding EGF-like growth factor (pro-HB-EGF) shedding and subsequent HB-EGF C terminal fragment signaling are related with progression of the cell cycle.
- ADAM12m is highly expressed in human glioblastomas and may play a role in the prominent proliferation of the glioblastomas through shedding of heparin-binding epidermal growth factor
- HB-EGF has a function in endometrial maturation in mediating decidualization and attenuating TNF alpha- and TGF beta-induced apoptosis of endometrial stromal cells.
- HB-EGF/HER-1 signaling is relevant to mesenchymal stem cell biology, by regulating both proliferation and differentiation
- These results suggested that HB-EGF in peritoneal fluid might play a key role in cell survival and in the proliferation of OVCA.
- HB-EGF may play a vital role in regulating luteal growth in a juxtacrine manner and through activating HER4 signalling
- HB-EGF is one of the factors that are significantly upregulated in PVR (proliferative vitreoretinopathy) retinas.
- Recombinant HB-EGF decreases proinflammatory cytokine-stimulated NF-kappa B activation and nitric oxide production via activation of the phosphoinositide-3-kinase signaling pathway.
- A post-transcriptional mechanism induced in trophoblasts by low O(2) rapidly amplifies HBEGF signaling to inhibit apoptosis.
- HB-EGF and amphiregulin mediate retinoic-acid induced epidermal hyperplasia
- results suggest a novel role for the cytoplasmic domain of HB-EGF that is regulated by phosphorylation
- lysophosphatidic acid-induced IL-8 secretion is partly dependent on EGFR transactivation regulated by PKCdelta-dependent activation of Lyn kinase and MMPs and proHB-EGF
- Inward potassium current in bladder urothelial cells(BUC) can be modulated by EGF and HB-EGF. Changes in BUC membrane potassium conductance caused by altered levels of EGF and HB-EGF may therefore play role in pathophysiology of interstitial cystitis.
- Glutamatergic neurotransmission plays a crucial role in regulating ectodomain shedding of transgenic HB-EGF in the brains of transgenic mice that overexpress human HB-EGF.
- Nardilysin has an essential role in HB-EGF ectodomain shedding, which is regulated by the modulation of sheddase activity
- Results demonstrate that mRNA stability and in particular the heparin binding epidermal growth factor like growth factor (HB-EGF) 3'-untranslated region is involved in HB-EGF mRNA induction.
- Chemotherapy-induced HB-EGF activation represents a critical mechanism of inducible chemotherapy resistance.
- HB-EGF carboxyl-terminal fragment is a potent regulator of gene expression via its interaction with the transcriptional repressor Bcl6.
- These findings demonstrate that amino-terminally truncated, membrane-bound form of HB-EGF stimulates cell proliferation but lacks insulin-like signalling.
- HB-EGF is up-regulated in tumor cells of SCC but not BCC of the skin. HB-EGF is also overexpressed in asymptomatic epidermis adjacent to both SCC and BCC, relative to normal skin.
- Gbetagamma mediates UVB-induced human keratinocyte apoptosis by augmenting the ectodomain shedding of HB-EGF, which sequentially activates EGFR and p38
- activation of PPARdelta is a major event in psoriasis, contributing to the hyperproliferative phenotype by induction of HB-EGF.
- The maintenance of the activation level of EGFR, which determines the cellular invasive potential, operates through an autocrine loop involving the JNK-dependent production of uPA and HB-EGF activity.
- Plasma/bladder concentrations of recombinant human rhHB-EGF equivalents were significantly lower following the intravesicular route than following intravenous administration. Histologic tissue examination indicated no toxicity attributable to rhHB-EGF.
- HB-EGF regulated epithelial repair is enhanced by IL-13 from airway epithelial cells
- Juxtacrine activation of EGFR by membrane-anchored HB-EGF may play an important role in the regulation of tight junction proteins and transepithelial resistance.
- alters the phenotype of keratinocytes in a manner similar to that observed during epidermal repair
- TNFalpha may play a key role in cooperation with HB-EGF and AREG in the proliferation of epidermal keratinocytes at the psoriatic skin lesions.
- HBEGF was present in almost all breast cancers studied. High expression is related to the biological aggressiveness of breast cancer.
- HB-EGF acts as a negative adipogenesis regulator during the early but not later stages of adipocyte differentiation, block the commitment of pluripotent mesenchymal cells to the adipocyte lineage triggered by bone morphogenic protein 4.
- Review. HB-EGF is implicated in angiogenesis, wound healing, blastocyst implantation, atherosclerosis, & tumor formation. It is the diphtheria toxin receptor.
- A novel hairless model on an atopic dermatitis-prone genetic background generated by DTR transgenesis is reported.
- HBEGF-mediated signaling significantly reduces trophoblast cell death at term and its deficiency in preeclampsia could negatively impact trophoblast survival.
- These results suggest that HB-EGF-Cys/Ser(134/143) antagonizes EGFRs.
- The roles of HB-EGF in cell adhesion, invasion, and angiogenesis in ovarian cancer, were examined.
- HB-EGF regulates endothelial cell function via stimulation of eNOS and nitric oxide production to promote eNOS dependent angiogenesis.
- Pro-inflammatory stimuli induce the release of HB-EGF from mesenchyme cells, which stimulates DNA-replication in initiated/premalignant hepatocytes