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抗Human Androgen Receptor 抗体:
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Human Monoclonal Androgen Receptor Primary Antibody for IHC (p), IHC - ABIN252555
Lin, Hu, Yang, Altuwaijri, Chen, Kang, Chang: Suppression versus induction of androgen receptor functions by the phosphatidylinositol 3-kinase/Akt pathway in prostate cancer LNCaP cells with different passage numbers. in The Journal of biological chemistry 2003
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Human Polyclonal Androgen Receptor Primary Antibody for ICC, IHC (p) - ABIN3044419
Xiang-Yun, Ying-Wen, Chen-Jing, Jiu-Jiu, Qi, Bo, Zu-Yue: Possible mechanism of benign prostatic hyperplasia induced by androgen-estrogen ratios in castrated rats. in Indian journal of pharmacology 2011
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Human Monoclonal Androgen Receptor Primary Antibody for IHC, ELISA - ABIN1724724
Tillman, Yuan, Gu, Fazli, Ghosh, Flynt, Gleave, Rennie, Kasper: DJ-1 binds androgen receptor directly and mediates its activity in hormonally treated prostate cancer cells. in Cancer research 2007
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Human Polyclonal Androgen Receptor Primary Antibody for IHC (p), ELISA - ABIN542902
Nishida, Yasuda: PIAS1 and PIASxalpha function as SUMO-E3 ligases toward androgen receptor and repress androgen receptor-dependent transcription. in The Journal of biological chemistry 2002
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Human Monoclonal Androgen Receptor Primary Antibody for ELISA, WB - ABIN968966
Lindström, Wiklund, Adami, Bälter, Adolfsson, Grönberg: Germ-line genetic variation in the key androgen-regulating genes androgen receptor, cytochrome P450, and steroid-5-alpha-reductase type 2 is important for prostate cancer development. in Cancer research 2006
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Human Monoclonal Androgen Receptor Primary Antibody for ELISA, WB - ABIN965588
Zong, Chi, Wang, Yang, Zhang, Chen, Jiang, Li, Hong, Wang, Yun, Gu: Cyclin D3/CDK11p58 complex is involved in the repression of androgen receptor. in Molecular and cellular biology 2007
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Human Monoclonal Androgen Receptor Primary Antibody for IHC (f), IHC (fro) - ABIN2688843
Fuller: The steroid receptor superfamily: mechanisms of diversity. in FASEB journal : official publication of the Federation of American Societies for Experimental Biology 1992
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Human Polyclonal Androgen Receptor Primary Antibody for IF (p), IHC (p) - ABIN725240
Madka, Mohammed, Li, Zhang, Biddick, Patlolla, Lightfoot, Towner, Wu, Steele, Kopelovich, Rao: Targeting mTOR and p53 Signaling Inhibits Muscle Invasive Bladder Cancer In Vivo. in Cancer prevention research (Philadelphia, Pa.) 2016
Polyclonal Androgen Receptor Primary Antibody for DB, IHC (fro) - ABIN540963
Ikeda, Aihara, Sato, Akaike, Yoshizumi, Suzaki, Izawa, Fujimura, Hashizume, Kato, Yagi, Tamaki, Kawano, Matsumoto, Azuma, Kato, Matsumoto: Androgen receptor gene knockout male mice exhibit impaired cardiac growth and exacerbation of angiotensin II-induced cardiac fibrosis. in The Journal of biological chemistry 2005
These findings demonstrate a novel working model in which EZH2 mediates AR-induced Wnt/beta-catenin signaling activation through epigenetic modification.
Our findings also suggest that prostate cancer cells may utilize AR, EGFR and MMP-9 pathways in androgen-dependent as well as in castration-resistant conditions. Our data suggest a new therapeutic potential to block cancer metastasis by targeting AR, EGFR and MMP-9 pathways in subsets of prostate cancer patients.
AR is an independent predictor of good prognosis in Breast Cancer , particularly in grade 3 and Luminal A tumours. Discordant AR-expression between primary tumour and lymph node metastases was observed in 21.4% of cases and most often there was a switch from AR(-) primary tumour to AR(+) axillary lymph node metastases .
AR expression heterogeneity is linked to distinct castration/enzalutamide responses in castration-resistant prostate cancer.
Androgen receptor positive triple negative breast cancer: Clinicopathologic, prognostic, and predictive features
In prostate cancer cells, AR-V7 expression is correlated with drug resistance, as AR-V7 upregulation leads to enhanced proliferation potency of cancer cells, indicating unfavorable prognosis of patients.
These findings imply that the deep intronic mutation creating an alternative splice acceptor site resulted in the production of a relatively small amount of wildtype androgen receptor mRNA, leading to partial androgen insensitivity syndrome.
AR Germline Mutations and Polymorphisms were associated with Prostate Cancer.
GTEE also downregulated the expression of AR and prostate-specific antigen (PSA) in both androgen-responsive and castration-resistant PCa cells. By blocking the SREBP-1/AR axis, GTEE suppressed cell growth and progressive behaviors, as well as activating the caspase-dependent apoptotic pathway in PCa cells
Suppressed the expression of androgen receptor.
An AR motif of the transactivation domain has been identified that contributes to transcriptional activity by recruiting the C-terminal domain of subunit 1 of the general transcription regulator TFIIF.
In LNCaP prostate cancer cells, TSG101 overexpression recruits the androgen receptor (AR) to TSG101-containing cytoplasmic vesicles resulting in reduced AR protein level and AR transactivation activity downregulation. Immunofluorescence microscopy demonstrated that TSG101-decorated cytoplasmic vesicles are associated with late endosomes/lysosomes.
Study indicates that both mRNA and protein level of AR increase during prostate cancer (PCa) progression. These levels are even higher in metastatic PCa. Further data suggest that elevation of AR may promote PCa metastasis by induction of EMT and reduction of KAT5.
This study aimed to determine the presence and localization of oestrogen receptors (ERs), progesterone receptors (PRs), and androgen receptors (ARs) in both healthy and varicose vein wall cells and their relationship with gender.
These findings suggest that CDK11 is involved in the regulation of AR pathway and AR can be a potential novel prognostic marker and therapeutic target for osteosarcoma treatment.
We use CPRC prostate cancer model and demonstrate that endothelial cells secrete large amount of CCL5 and induces autophagy by suppressing AR expression in prostate cancer cell lines. Consequently, elevated autophagy accelerates focal adhesions proteins disassembly and promoted prostate cancer invasion. Inhibition of both CCL5/CCR5 signaling and autophagy significantly reduces metastasis in vivo
Overexpression of nuclear AR-V7 protein identifies a subset of tumors with remarkably aggressive growth characteristics among clinically and histologically high-risk patients at the time of radical prostatectomy.
Study defines AR ligand-binding domain homodimerization as an essential step in the proper functioning of this important transcription factor. Dimerization surface harbours over 40 previously unexplained androgen insensitivity syndromes and prostate cancer-associated point mutations.
Loss of AR expression was found in the nucleus of penile cancer cells when compared to normal tissues. Cytoplasmic AR immunostaining was observed in a significant number of these cases and was related with poor prognosis and shorter overall survival.
The AR polymorphism is associated with POR risk, patients with repeats greater than 22 show a higher risk. Our data suggest that AR genotype could play a role in natural ovarian aging.
Here, the authors show that ERG, through its physical interaction with androgen receptor, induces AR aggregation and endoplasmic reticulum stress in the prostate glands of ERG transgenic mice.
CSN6 and Rab34 are involved in AR trafficking by regulating the phosphorylation signaling pathway. These findings provide new insights into the testosterone signaling pathway in Sertoli cells that mediates spermatogenesis.
Results provide evidence that androgen receptor is expressed from prenatal stages in mouse heart, supporting the proposition that androgens could be involved in mammalian heart development.
Androgens act via non-neural AR to mediate olfactory preference and neural responses to olfactory stimuli, and further, AR in non-neural tissues can promote androphilic odor preferences in male mice.
The role of ERbeta in opposing AR signaling, proliferation, and inflammation suggests that ERbeta-selective agonists may be used to prevent progression of prostate cancer, prevent fibrosis and development of benign prostatic hyperplasia, and treat prostatitis.
androgen receptor has a central role in the spontaneous regeneration of myelin
Data (including data from studies using transgenic/knockout mice) suggest that AR in insulin-secreting cells is involved in insulin secretion and inflammation; AR-deficient insulin-secreting cells exhibit altered expression of genes involved in inflammation and insulin secretion demonstrating importance of androgen action in functions of insulin-secreting cells.
Cyclic mechanical stretch modulated the proliferation of C2C12 cells, which may be attributed to the alterations of AR via IGF-1-PI3K/Akt and IGF-1-MAPK (p38, ERK1/2) pathways in C2C12 cells.
We show AR expressed in cancer-associated fibroblasts (CAFs) contributes to the tumor-promoting abilities that CAFs exert on epithelial prostate cancer cells. Further, we found that decreased AR expression in CAFs is also associated with an increase in stem cell marker gene expression in prostate cancer epithelial cells.
in clear cell renal cell carcinoma, enhances lung and liver metastases, while suppressing lymphatic metastasis
The results indicate that AR expression may be the gatekeeper of postoperative hepatocellular carcinoma recurrence
Glandular epithelial AR inactivation (with persistent stromal AR action) enhanced PTEN deletion-induced uterine pathology possibly by downregulating progesterone receptor expression in the uterus.
CDK2 phosphorylates polyQ-AR specifically at Ser(96). Phosphorylation of polyQ-AR by CDK2 increased protein stabilization and toxicity and is negatively regulated by the adenylyl cyclase/protein kinase A signaling pathway in spinobulbar muscular atrophy.
experimental manipulation of the prenatal androgen level, by blocking the androgen receptor with flutamide or activating the androgen receptor with dihydrotestosterone (DHT), leads to changes in the length of the fingers of all paws in males and females.
Silencing of androgen receptor rescues the muscular spinal atrophy transgenic mice.
Taken together, our findings provide evidence for a novel crosstalk and a crossregulation between ING1 and ING2 in regulating androgen receptor-mediated transactivation and suggest that ING2 acts as a novel corepressor that inhibits AR signaling, prostate cancer cell growth, and migration.
Data provide evidence for a role of androgens via the AR in neurons to positively regulate fast-twitch hind-limb muscle mass and physical activity in male mice.
AR binds Sox2OT response elements in embryonic brain.
Prostate 5aR1 levels were positively correlated with adjusted prostate most severe lesion scores. Downregulation of androgen receptor and 5alpha-reductase 2, along with upregulation of 5a-reductase 1 in tumors may promote prostatic intraepithelial neoplasia and prostate cancer development in TRAMP mice
Disrupting luminal cell AR signaling in mouse models promotes cytokine production cell-autonomously, impairs epithelial barrier function, and induces immune cell infiltration.
substantial up-regulation of androgen receptor expression during trophoblast giant cell differentiation suggests that androgens may be related to this process and are active products of bovine placental steroidogenesis
no association between the AR CAG polymorphism and the relative risk of prostate cancer in white Brazilian individuals with a CAG repeat
FSHR is specifically regulated through androgen receptor in granulosa cells
Roles of IGF-I and the estrogen, androgen and IGF-I receptors in estradiol-17beta- and trenbolone acetate-stimulated proliferation of cultured bovine satellite cells.
In GD20 and PD2 males we found the reduction of the luminal compartment, inflammatory changes, decreased androgen receptor and increased Cx43 expression
Data suggest that signal transduction involving androgen receptor is involved in apoptosis of granulosa cells (as seen in follicular atresia).
AR is a potential candidate gene for traits related to pig reproduction and performance
presence of AR during gestation in non-gonadal tissues suggests a role of androgen in these tissues
Pig ejaculated spermatozoa express androgen receptor.
Androgen receptor (AR) and Wilms' tumor gene 1 expression dramatically decreased after heat treatment in Sertoli cells
Zebrafish males lacking the androgen receptor courted females significantly less, showing reduced levels of stereotypic behaviors. Consistent with previous studies, disrupting androgen mechanisms can lead to behavioral changes with potential fitness consequences.
AR regulates sexual determination, testis development, and oocyte maturation and AR regulates sexually dimorphic gene expression. The ar mutant developed will be useful for modeling human endocrine function in zebrafish.
Findings suggest that zebrafish embryos attempt to compensate for the presence of an anti-androgen by increasing the number of androgen receptors available.
The isolation and characterization of zebrafish Ar were reported.
ar was expressed in discrete regions of the telencephalon, in the preoptic area, and throughout the periventricular hypothalamus, regions previously implicated in the regulation of sexually dimorphic behaviors in mammals
Sertoli cell maturation during puberty in the stallion was accompanied by a reduced expression of anti-Mullerian hormone and its receptor, arrest of cell proliferation, increased expression of androgen receptor
The vesicular gland of castrated goats showed significantly lower AR and COX-2 immuno-expression than intact goats indicating that both AR and COX-2 are androgen dependent.
The androgen receptor gene is more than 90 kb long and codes for a protein that has 3 major functional domains: the N-terminal domain, DNA-binding domain, and androgen-binding domain. The protein functions as a steroid-hormone activated transcription factor. Upon binding the hormone ligand, the receptor dissociates from accessory proteins, translocates into the nucleus, dimerizes, and then stimulates transcription of androgen responsive genes. This gene contains 2 polymorphic trinucleotide repeat segments that encode polyglutamine and polyglycine tracts in the N-terminal transactivation domain of its protein. Expansion of the polyglutamine tract causes spinal bulbar muscular atrophy (Kennedy disease). Mutations in this gene are also associated with complete androgen insensitivity (CAIS). Two alternatively spliced variants encoding distinct isoforms have been described.
androgen nuclear receptor variant 2
, dihydrotestosterone receptor
, nuclear receptor subfamily 3 group C member 4
, testicular feminization
, androgen receptor (Testicular feminization), same as Tfm
, androgen receptor (dihydrotestosterone receptor; testicular feminization; spinal and bulbar muscular atrophy; Kennedy disease)
, androgen receptor AR
, Ar beta
, androgen receptor
, prostate androgen receptor