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Validated All-in-One™ qPCR Primer for ERBB4(NM_005235.3) Search again
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.
Summary
This gene is a member of the Tyr protein kinase family and the epidermal growth factor receptor subfamily. It encodes a single-pass type I membrane protein with multiple cysteine rich domains, a transmembrane domain, a tyrosine kinase domain, a phosphotidylinositol-3 kinase binding site and a PDZ domain binding motif. The protein binds to and is activated by neuregulins and other factors and induces a variety of cellular responses including mitogenesis and differentiation. Multiple proteolytic events allow for the release of a cytoplasmic fragment and an extracellular fragment. Mutations in this gene have been associated with cancer.
Gene References into function
- cleavage by gamma-secretase releases the ErbB-4 intracellular domain from the membrane and facilitates its translocation to the nucleus
- ErbB4 expression was observed through all stages of chondrocytic differentiation in vitro.
- deletion of the PDZ domain recognition motif does abrogate the gamma-secretase cleavage of ErbB-4
- ErbB4 is specifically associated with neuritic plaques in the hippocampus of Alzheimer disease patients.
- ErbB4 signaling is growth inhibitory and may be coupled to tumor suppression in prostate cells
- Expression of HER4 protein correlates with favourable tumor stage in pancreatic cancer patients.
- YAP is a potential signaling partner of the full-length ErbB4 receptor at the membrane and of the COOH-terminal fragment of ErbB-4 that translocates to the nucleus to regulate transcription
- ErbB-4 characterization of the cleavage site and m80 fragment
- Nuclear localization of the activated p80 fragment of Her-4 is associated with osteosarcoma pathogenesis
- HER4 is involved in a non-proliferative or even protective role in breast cancer.
- betacellulin may play a role as a local growth factor in promoting the differentiated villous trophoblastic function via ErbB-1 in early placentas and in contributing to placental growth through EVT cell function via ErbB-4 in term placentas.
- nuclear localization of STAT5A and stimulation of the beta-casein promoter requires nuclear translocation of the ERBB4 intracellular domain 4ICD; binding of the two proteins at transcription factor target promoters results in activation of gene expressio
- ErbB4 is increased by cAMP, a potent inducer of decidualization of the endometrial stroma.
- erbB receptor inactivation by unknown mechanisms results in altered splicing of bcl-x towards enhanced formation of proapoptotic Bcl-xS, thereby contributing to enhanced apoptotic susceptibility of failing human myocardium
- Association of ErbB4 expression with clinical outcome is dependent on the subcellular localization of ErbB4 and that a proteinase-cleavable ErbB4 isoform promotes growth of ER-positive breast cancer and enhances ER-mediated gene transcription.
- proteolytic processing of ERBB4 is a critical event regulating multiple receptor signaling activities
- Absence of HER4 expression is associated with recurrence of ductal carcinoma in situ of the breast
- HB-EGF may play a vital role in regulating luteal growth in a juxtacrine manner and through activating HER4 signalling
- Data show that expression of the ErbB-4 ICD fragment leads to its constitutive association with and tyrosine phosphorylation of Mdm2.
- WWOX antagonizes the function of YAP by competing for interaction with ErbB-4 and other targets and thus affect its transcriptional activity.
- the s80 domain of ErbB-4 may function to phosphorylate substrates in the cytoplasm or nucleus
- Data suggested that alterations of ERBB4-mediated signaling pathway by ERBB4 mutations may contribute to the development of human cancers.
- Results report the 2.4 A crystal structure of the extracellular region of human ErbB4 in the absence of ligand and show that it adopts a tethered conformation similar to inactive forms of ErbB1 and ErbB3.
- Mutation screening of erbB4 in 14 schizophrenics revealed 15 SNPs.
- novel transforming mechanism for the ErbB4 receptor in human breast cancer that is 1) specific for a single receptor isoform and 2) depends on proteinase cleavage and kinase activity but not ligand activation of the receptor
- Results showed a highly significant difference between patient and control groups in three SNPs from one linkage disequilibrium block both in allele and genotype frequencies, as well as a risk haplotype.
- Activation of Rac by heregulin beta1 is mediated not only by ErbB3 and ErbB2 but also by transactivation of EGFR, and it is independent of ErbB4.
- A monoclonal antibody to ErbB-4 showed both an inhibitory effect on growth rate and an increasing apoptotic rate in the cells expressing ErbB-4.
- ErbB4 receptor expression was accompanied with positive regulation of PP2A for phosphorylation of Shc Tyr317 and its downstream ERK phosphorylation in MCF-7 and SK-OV-3 cell lines, but not in LNCaP and PC-3 cells.
- These experiments demonstrate a novel mechanism controlling ErbB receptor activation. Ras induces ErbB4 receptor phosphorylation in a non-autocrine manner and this activation depends on multiple Ras effector pathways and on ErbB4 kinase activity.
- Function of HER4 and its fragments is particularly important, with he different functions of nuclear and mitochondrial HER4 in breast cancer.
- HER3 and HER4 has been related to a favourable prognosis in bladder cancer.
- ErbB4 has 5 docking sites for Grb2. It is a direct binding partner for STAT5. It functions as control center & integration site for signaling processes, involving stimulation with neuregulin.
- Neurogulin 1 induced activation of erbB4 in the prefrontal cortex in schizophrenia.
- Cytosolic but not membrane ERBB4/4ICD expression in primary human breast tumors was associated with tumor apoptosis, providing a mechanistic explanation for the loss of ERBB4 expression during tumor progression.
- -16 E5 protein can form a complex with ErbB4 via binding to the extracellular and transmembrane domains of ErbB4 (JM-b/CYT-1)
- Down regulation of ERBB4 is associated with brease, prostate and ovarian cancer
- Expression of c-erbB-4 in brain medulloblastoma and its correlation with prognosis.
- low-level hedgehog signalling in human medulloblastoma is associated with the selective maintenance of high ErbB-4 CYT-1 expression, an alteration that exerts tumor-promoting effects
- Contribution of an autocrine ERBB4/estrogen receptor signaling pathway to tumor growth and therapeutic response should be considered when managing patients with ER-positive breast cancer.
- These results suggest that heregulin-mediated growth inhibition in HER4-postive breast cancer cells requires BRCA1.
- phosphorylation of ErbB4 tyrosine 1056 is critical for coupling ErbB4 to prostate tumor suppression
- Data show that upon neuregulin-induced activation and presenilin-dependent cleavage of ErbB4, the receptor's intracellular domain forms a complex with TAB2 and the corepressor N-CoR.
- Dysregulation of splice-variant specific expression of ErbB4 in the brain underlies the genetic association of the gene with schizophrenia.
- Inhibits mammary cell proliferation through the action of its cytoplasmic domain.
- cycle-dependent degradation of s80(HER4) limits its growth-inhibitory action, and stabilization of s80(HER4) enhances tumor suppression, thus providing a link between HER4-mediated growth inhibition and cell cycle control
- study concludes that erbB4 mutations are rare in Japanese people with lung cancer
- ErbB4 isoform that is proteinase cleavable but does not contain a PI3K-binding domain in its cytoplasmic tail, mediates important functions in renal epithelial cells in response to HB-EGF
- Expression of Wwox is associated with ErbB4 expression and that their coexpression has prognostic significance in breast cancer.
- Gln43 of NRG2beta is both necessary and sufficient for NRG2 stimulation of ErbB4 coupling to IL3 independence.
- The ERBB4 -782 G>T polymorphism, by virtue of its in vitro functional implication and incidence, is a risk factor for breast and colorectal cancer.
- HER4 amplification showed a positive trend in overall and disease-free survival.
- All ErbB4 residues contacted by lapatinib are conserved in the EGF receptor and HER2/ErbB2, which lapatinib also targets.
- Ras activation dynamics is dominated by heterodimer-mediated signaling coordination with a large initial speed of dimerization when the concentration of the ErbB4 receptor is considerably high
- Her 4 expression showed significantly decreased expression in differentiated throid cancer and correlated with lower T stage
- The restriction of robust SVZ ErbB4 expression to neonate and infant age groups may indicate that SVZ-derived ErbB4-dependent postnatal neuronal development is most extensive within a narrow time frame early after birth.
- several previously unrecognized interactions led to the finding that ErbB4 can recruit and activate STAT1; at a systems level, ErbB4 is much more selective than the other ErbB receptors
- ErbB4 expression and signaling are key elements for TNF responses in vivo and in cell culture, protecting intestinal epithelial cells from apoptosis in the inflammatory environment.
- HER3 and HER4 gene transcription is associated with better prognosis in high-risk early breast cancer
- The biological function and clinical implications of HRG, HER-3 and HER-4 in breast cancers negative/low expression of HER-2 remain unclear
- Removal of cell surface heparan sulfate increased TACE activity and cleavage of ErbB4 receptor.
