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- Table of Contents
Facts about Receptor tyrosine-protein kinase erbB-4.
Required for normal development of the embryonic central nervous system, especially for normal neural crest cell migration and normal axon guidance. Required for mammary gland differentiation, induction of milk proteins and lactation.
Human | |
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Gene Name: | ERBB4 |
Uniprot: | Q15303 |
Entrez: | 2066 |
Belongs to: |
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protein kinase superfamily |
avian erythroblastic leukemia viral (v-erb-b2) oncogene homolog 4; EC 2.7.10; EC 2.7.10.1; ErbB4; HER4; HER4MGC138404; p180erbB4; Proto-oncogene-like protein c-ErbB-4; receptor tyrosine-protein kinase erbB-4; Tyrosine kinase-type cell surface receptor HER4; v-erb-a avian erythroblastic leukemia viral oncogene homolog-like 4; v-erb-a erythroblastic leukemia viral oncogene homolog 4 (avian)
Mass (kDA):
146.808 kDA
Human | |
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Location: | 2q34 |
Sequence: | 2; NC_000002.12 (211375717..212538802, complement) |
Expressed at highest levels in brain, heart, kidney, in addition to skeletal muscle, parathyroid, cerebellum, pituitary, spleen, testis and breast. Lower levels in thymus, lung, salivary gland, and pancreas. Isoform JM-A CYT-1 and isoform JM-B CYT-1 are expressed in cerebellum, but only the isoform JM-B is expressed in the heart.
Cell membrane; Single-pass type I membrane protein. In response to NRG1 treatment, the activated receptor is internalized.; [ERBB4 intracellular domain]: Nucleus. Mitochondrion. Following proteolytical processing E4ICD (E4ICD1 or E4ICD2 generated from the respective isoforms) is translocated to the nucleus. Significantly more E4ICD2 than E4ICD1 is found in the nucleus. E4ICD2 colocalizes with YAP1 in the nucleus.
If you've ever wondered how ERBB4 works, you're in the right spot. Boster Bio has extensive knowledge of this marker, as well the various functions it performs in the body. This article focuses on ERBB4, PI3K or EGFR. To further your research, learn how to use these antibodies. Information about p-AKT and b-actin as well as EGFR will be provided.
The ERBB4 receptor marker is a crucial member of the EGF family. This tyrosinekinase functions as a shared receptor with ErbB2 and has no direct ligand. It is frequently overexpressed in breast cancer. Recent clinical trials of humanized antibodies against ErbB2 showed that they have a cytostatic effect on 40% of ErbB2-positive breast tumor cells.
Recent research has shown that MSCs with ERBB4 overexpression can increase survival after myocardial injury. Researchers used genetic manipulations in order to alter the expression levels of this gene in MSCs. The results showed that ERBB4 significantly boosted cardiomyocyte survival. Despite the varying levels ERBB4 protein, the results showed no significant differences between MSCe vs MSCe.
ERBB4 was also expressed in MSCs, which improved cardioprotection as well as preserved cardiomyocyte functions. The study also found that ERBB4 was overexpressed in MSCs, which increased the survival rate of cardiomyocytes and stimulated the division of cardiomyocytes. The gene was also found to have cardioprotective properties in mice after myocardial ischemia.
Cancer therapy is based on the inhibition of ERBB3. It is well known to regulate downstream signaling pathways that regulate cancer growth. Cancer cells cannot spread and migrate if this gene is blocked. The prevention of cancer and survival rates can be improved by inhibiting ERBB3 and ERBB4. Recent research revealed that this gene was associated with a number human malignancies.
Inhibition of ERBB4 reduces cardiomyocyte proliferation. It also causes cytokinesis in cardiomyocytes. Postnatal activity of the cardiomyocyte cell-cycle is abolished by ErbB4 activation. Therefore, a positive association between this gene and cardiomyocyte proliferation may be observed. ERBB4 is a key player in cardiomyocyte proliferation.
Differentiation has also been linked with the miR-146a-5p genetic. It targets ErbB4's gene and regulates ERK's activity. It is also linked to adipogenesis. Overexpression of ERBB4 results in the inhibition of 3T3L1 cell proliferation and a decrease in intracellular lipid droplet levels. Moreover, ERBB4 is overexpressed which reduces TG.
Gefitinib combined with PI103 reduces the proliferation and growth of BL, MDA-MB-468, and other cell lines. The drugs had no or very little effect on cell lines that are resistant EGFRi. In this subtype of TNBC, PI3K/ERBB4 inhibition is an important therapeutic approach. Combining these two drugs could have anti-tumor properties in these cells.
The EGFR is an epidermal growth factor receptor. It is a common target for cancer therapy. This article will discuss how this gene is used to treat non-small cell lung carcinoma. We will first discuss EGFR and how it can help identify cancer cells. The cellular receptor for epidermal Growth Factor is the EGFR marker.
The EGFR marker is a diagnostic method that is used for the diagnosis of lung cancer. It can be used to prognostically in postoperative patients and predict response to cytotoxic therapy. This test can also help predict the outcome for patients with EGFR variants. A recent study by Marks et. al45 found that patients with EGFR mutations had better outcomes compared to patients with KRAS mutations.
EGFR ELISAKits can be used as a screening tool to detect EGFR in cultured cell lines. The ELISA Kits provide a convenient and high-throughput way for researchers to monitor EGFR expression in cultured cells. Researchers can monitor the effects on various treatments with the ELISA Kit, including activators and inhibitors.
The EGFR gene is an oncogenic one that controls many types of tumors. It plays an important role in the development tumors, including lung carcinoma. There are many ways to treat cancer with this gene. Most of the EGFR inhibitors are effective for months or years. The cancer develops resistance to drugs as it adapts to them. To determine which drug is best for you, biomarker tests are helpful.
Although the research was retrospective in nature the EGFR gene mutation is directly linked with survival in patients diagnosed with NSCLC. Clinicians can now better decide the best treatment for each patient's condition using this information. The EGFR mutation is an intrinsic marker for tumor progression and has a direct relation to the end result. Physicians can now make better decisions about NSCLC treatment thanks to this new information.
Another study found that patients with the EGFR mutation p.T790M had a longer PFS and OS than patients with the wild-type gene. Patients with a p.T790M mutation had a longer PFS, and OS than those with other EGFR mutations. It is also important that patients with p.T790M EGFR Mutations are more susceptible to treatment with EGFRTKIs.
There are several reasons to use the EGFR-mutated gene. It has been shown useful in the management of patients with advanced NSCLC. There are many available cancer drugs. However, EGFR inhibitors can become resistant and may not be able to control the growth of tumors. BerGenBio can help. By identifying the EGFR mutation in cancer cells, it can target the cancer cell and prevent its growth.
PMID: 8383326 by Plowman G.D., et al. Ligand-specific activation of HER4/p180erbB4, a fourth member of the epidermal growth factor receptor family.
PMID: 9334263 by Elenius K., et al. A novel juxtamembrane domain isoform of HER4/ErbB4. Isoform-specific tissue distribution and differential processing in response to phorbol ester.