抗Human Amphiregulin 抗体:
抗Mouse (Murine) Amphiregulin 抗体:
抗Rat (Rattus) Amphiregulin 抗体:
Human Polyclonal Amphiregulin Primary Antibody for IF (p), IHC (p) - ABIN704996
Jiang, Song, Li, Guo, Wu, Li, Guo, Shi, Bi, Jonas: Amphiregulin Antibody and Reduction of Axial Elongation in Experimental Myopia. in EBioMedicine 2017
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Human Polyclonal Amphiregulin Primary Antibody for WB - ABIN6746007
Chen, Parsons, Brautigan: Tyrosine phosphorylation of protein phosphatase 2A in response to growth stimulation and v-src transformation of fibroblasts. in The Journal of biological chemistry 1994
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Human Polyclonal Amphiregulin Primary Antibody for IHC, IHC (p) - ABIN4280428
Barton, DAmato, Gordon, Lind, Spoelstra, Babbs, Heinz, Elias, Jedlicka, Jacobsen, Richer: Multiple molecular subtypes of triple-negative breast cancer critically rely on androgen receptor and respond to enzalutamide in vivo. in Molecular cancer therapeutics 2015
Human Polyclonal Amphiregulin Primary Antibody for IHC, IHC (p) - ABIN4280429
Raimondo, Saieva, Vicario, Pucci, Toscani, Manno, Raccosta, Giuliani, Alessandro: Multiple myeloma-derived exosomes are enriched of amphiregulin (AREG) and activate the epidermal growth factor pathway in the bone microenvironment leading to osteoclastogenesis. in Journal of hematology & oncology 2019
We concluded that YAP may play an important role in the regulation of abnormal keratinocyte proliferation via an AREG-dependent pathway and that YAP could be a new target in the treatment of psoriasis.
AREG and EREG mRNA expression levels in left-sided CRC were higher than in right-sided tumors. This may help explain why left-sided CRC is more responsive to anti-EGFR antibodies.
FOSL1 is a determinant of lung cancer in vivo and regulates tumor cell proliferation and survival, largely in the context of KRAS mutations through amphiregulin and cell survival gene regulation.
Treatment with lapatinib reduced BeWo cell proliferation by inducing apoptosis. Moreover, AREG treatment stimulated BeWo cell proliferation by activating ERK1/2 and PI3K/AKT signaling pathways, which was blocked by lapatinib. Targeting EGFR/HER2 might be a useful therapeutic strategy for human choriocarcinoma
Data showed that AR was highly expressed and secreted in mobile and Doxorubicin (Dox)-resistant cells. AR can promote migratory activity and Dox resistance through activation of the MAPK pathway.
Retrospective comparison of the predictive power of AREG gene-body methylation versus AREG gene expression using samples from colorectal cancer patients treated with anti-EGFR inhibitors with complete clinical follow-up revealed that AREG expression is superior to AREG gene methylation.
We found that CRB3-induced proliferation is epidermal growth factor (EGF)-independent and occurs through a mechanism that involves secretion of the EGF-family ligand, amphiregulin (AREG)..We identified the FBD-containing protein, EPB41L4B, as an essential mediator of CRB3-driven proliferation and observed that the CRB3-dependent changes in endocytic trafficking were also dependent on EPB41L4B
High-circulating AREG (>/=33 pg/mL) reclassifies patients into HR subgroups and thereby further refines the Minnesota aGVHD clinical risk score.
Results show that Areg is involved in the nuclear accumulation of IGF1R induced by gefitinib and preventing the induction of apoptosis of lung cancer cells.
These results indicate that AR occurs through the Src/MEK/ERK/STAT-3 pathway, activating VEGF-C expression and contributing to lymphangiogenesis in human chondrosarcoma. Thus, AR could be a therapeutic target in metastasis and lymphangiogenesis of chondrosarcoma.
Whole genome bisulfite sequencing revealed that integrin alpha6beta4 signaling promotes an overall hypomethylated state and site specific DNA demethylation of enhancer elements within the proximal promoters of AREG and EREG in pancreatic neoplasm cells as well as their expression. Additionally, base excision repair (BER) pathway is required to maintain the expression of AREG and EREG.
Amphiregulin contained in non-small-cell lung carcinoma-derived exosomes induces osteoclast differentiation through the activation of EGFR pathway.
The studies indicate that HIF2-alpha induces myocardial AREG expression in cardiac myocytes, which increases myocardial ischemia tolerance.
AREG mediates hCG-induced StAR expression and progesterone production in human granulosa cells, providing novel evidence for the role of AREG in the regulation of steroidogenesis.
Regulatory T-cell-intrinsic amphiregulin is dispensable for suppressive function.
No significant correlations emerged for YAP or AREG expression and VIII CN schwannoma volume.
Cullin 3 regulates ADAM17-mediated ectodomain shedding of AREG.
over-expression of AREG could serve as a novel GC biomarker, and active surveillance of its expression could be a novel approach to GC diagnosis and monitoring.
Sprouty2 inhibits amphiregulin-induced down-regulation of E-cadherin and cell invasion in human ovarian cancer cells.
Results show that AREG expression is up-regulated in gastric tumor and its co-expression with TROP2 protein is associated with TNM stage, tumor size, lymph node metastases, and distant metastases.
Study using murine luminal B breast cancer model, MMTV-PyMT crossed to Areg-knockout mice has revealed a previously unknown role of Areg in myoepithelial cell development and PyMT expression. Areg expression is essential for proper myoepithelial coverage of mammary ducts. Both Areg and myoepithelial cells can suppress PyMT expression.
these results imply that IL-18 may participate in controlling the severity of stromal keratitis and contribute to tissue repair by converting both Treg and effector T cells into those that produce Amphiregulin.
These data show that elevated levels of testosterone and AREG, either independently or in combination, improve resilience (i.e., repair and recovery of damaged tissue) and contribute to better influenza outcomes in males compared with females.
Amphiregulin production is enhanced by the IL-33 receptor, ST2(hi) memory T helper 2 (Th2) cells. Amphiregulin-epidermal growth factor receptor (EGFR)-mediated signaling reprogram eosinophils to an inflammatory state with enhanced production of osteopontin. IL-5-producing memory Th2 cells and amphiregulin-producing memory Th2 cells cooperate to establish lung fibrosis.
Amphiregulin plays an important role in promoting cardiac fibrosis after myocardial infarction partly though activating the EGFR pathway.
Areg transgenic mice showed less adipose tissue mass with increased mRNA expression levels of Tnf-alpha and peroxisome proliferator-activated receptor gamma coactivator 1 alpha and delayed white adipose tissue development during the convalescent stage in a dextran sodium sulfate-induced colitis model.
activated alveolar macrophages also exerted a protective effect on the lung tissues by producing high-level amphiregulin in lipopolysaccharide-induced acute lung injury
AREG overexpression in osteoblasts induces a transient high bone mass phenotype in the trabecular compartment of the appendicular skeleton by a growth-related, non-cell autonomous mechanism
AREG-silenced keratinocytes plays an important role in regulation cell proliferation.
Hepatic CD206-positive macrophages express amphiregulin to promote the immunosuppressive activity of regulatory T cells in HBV infection.
Areg may have a role in classically activated macrophages
After activation with IL-33, expression of AREG is a dominant functional signature of gut-associated IL-33-dependent group 2 innate lymphoid cells. The frequency and number of AREG-expressing ILC2s increases following intestinal injury.
AR induces hHSC fibrogenic activity via multiple mitogenic signaling pathways, and is upregulated in murine and human NASH, suggesting that AR antagonists may be clinically useful anti-fibrotics in NAFLD.
hormones and/or factors in addition to E that upregulate AREG can promote mammary gland development and have the potential to affect breast cancer risk associated with pubertal mammary gland development
Our data show that AREG is essential for ultraviolet therapy-induced contact hypersensitivity suppression.
Pre-maturation with cAMP modulators in conjunction with EGF-like peptides during in vitro maturation enhances mouse oocyte developmental competence.
During high-pressure ventilation, Nrf2 becomes activated and induces AREG, leading to a positive feedback loop between Nrf2 and AREG, which involves the p38 MAPK and results in the expression of cytoprotective genes.
LH and AREG decrease BNP and CNP production in granulosa cells and down-regulate NPR2 expression in cumulus cells, which together decreased oocyte cGMP to levels that permit meiotic resumption.
cloning the complete coding region; comparison of endometrial amphiregulin mRNA expression in Meishan and White composite pigs
Amphiregulin co-operates with bone morphogenetic protein 15 to increase bovine oocyte developmental competence.
Data suggest that epidermal growth factor receptor B [ErbB] isoforms and their ligands (epidermal growth factor [EGF], amphiregulin [AREG], and neuregulin-1 [NRG1]) are expressed in uteroplacental tissues in mid- and late-phases of pregnancy.
The protein encoded by this gene is a member of the epidermal growth factor family. It is an autocrine growth factor as well as a mitogen for astrocytes, Schwann cells, and fibroblasts. It is related to epidermal growth factor (EGF) and transforming growth factor alpha (TGF-alpha). This protein interacts with the EGF/TGF-alpha receptor to promote the growth of normal epithelial cells and inhibits the growth of certain aggressive carcinoma cell lines. This encoded protein is associated with a psoriasis-like skin phenotype.
colorectum cell-derived growth factor
, schwannoma-derived growth factor
, amphiregulin (schwannoma-derived growth factor)
, amphiregulin long form
, amphiregulin B
, Schwannoma-derived growth factor