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           Search results for: Androgen Receptor (Phospho-Ser213) Antibody   

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Increase Paclitaxel Sensitivity to Better Suppress Serous Epithelial Ovarian Cancer via Ablating Androgen Receptor/Aryl Hydrocarbon Receptor-ABCG2 Axis.

Epithelial ovarian cancer (EOC) is one of the most lethal gynecological malignancies and presents chemoresistance after chemotherapy treatment. Androgen receptor (AR) has been known to participate in proliferation. Yet the mechanisms of the resistance of this drug and its linkage to the AR remains unclear.

2828 related Products with: Increase Paclitaxel Sensitivity to Better Suppress Serous Epithelial Ovarian Cancer via Ablating Androgen Receptor/Aryl Hydrocarbon Receptor-ABCG2 Axis.

Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Rat Toll Like Receptor 2( Rat Toll Like Receptor 6( Androgen Receptor (Ab 650 anti Transferrin receptor AZD-3514 Mechanisms: Andr Dog Receptor-binding canc Rabbit Anti-Human Androge Goat Anti-Human Androgen

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The gonadotropin-inhibitory hormone system of fish: The case of sea bass (Dicentrarchus labrax).

Gonadotropin-inhibitory hormone (GnIH) is a hypothalamic neuropeptide belonging to the RFamide peptide family that was first discovered in quail by Tsutsui and co-workers in the year 2000. Since then, different GnIH orthologues have been identified in all vertebrate groups, from agnathans to mammals. These GnIH genes synthesize peptide precursors that encompass two to four C-terminal LPXRFamide peptides. Functional and behavioral studies carried out in birds and mammals have demonstrated a clear inhibitory role of GnIH on GnRH and gonadotropin synthesis and secretion as well as on aggressive and sexual behavior. However, the effects of Gnih orthologues in reproduction remain controversial in fish with both stimulatory and inhibitory actions being reported. In this paper, we will review the main findings obtained in our laboratory on the Gnih system of the European sea bass, Dicentrarchus labrax. The sea bass gnih gene encodes two putative Gnih peptides (sbGnih1 and sbGnih2), and is expressed in the olfactory bulbs/telencephalon, diencephalon, midbrain tegmentum, rostral rhombencephalon, retina and testis. The immunohistochemical study performed using specific antibodies developed in our laboratory revealed Gnih-immunoreactive (ir) perikarya in the same central areas and Gnih-ir fibers that profusely innervated the brain and pituitary of sea bass. Moreover, in vivo studies revealed the inhibitory role of centrally- and peripherally-administered Gnih in the reproductive axis of male sea bass, by acting at the brain (on gnrh and kisspeptin expression), pituitary (on gnrh receptors and gonadotropin synthesis and release) and gonadal (on androgen secretion and gametogenesis) levels. Our results have revealed the existence of a functional Gnih system in sea bass, and have provided evidence of the differential actions of the two Gnih peptides on the reproductive axis of this species, the main inhibitory role in the brain and pituitary being exerted by the sbGnih2 peptide. Recent studies developed in our laboratory also suggest that Gnih might be involved in the transduction of photoperiod and temperature information to the reproductive axis, as well as in the modulation of daily and seasonal rhythmic processes in sea bass.

2122 related Products with: The gonadotropin-inhibitory hormone system of fish: The case of sea bass (Dicentrarchus labrax).

FDA Standard Frozen Tissu Normal rat multiple organ Normal rat multiple organ Normal rat multiple organ Multiple organ cancer tis Multiple organ tumor tiss Tissue array of ovarian g BACTERIOLOGY BACTEROIDES TCP-1 theta antibody Sour Recombinant Thermostable Recombinant Thermostable Recombinant Thermostable

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Nimotuzumab inhibits epithelial-mesenchymal transition in prostate cancer by targeting the Akt/YB-1/AR axis.

Nimotuzumab is a humanized anti-EGF monoclonal antibody that has been approved for treating different cancers. However, few studies have examined its therapeutic potential in prostate cancer (PC), a most common and highly aggressive malignancy among male population. We used both LNCaP, and PC3 and PC3-AR (androgen receptor) cells as the model system and assessed the effects of nimotuzumab on epithelial-mesenchymal transition (EMT) in vitro and in vivo. The EMT makers were detected by immunohistochemistry, qRT-PCR and Western blot. MTT, wound healing assay, and transwell assay were used to measure cell viability, migration, and invasion, respectively. For mechanistic understanding, we evaluated the significance of Akt/Y-box binding protein-1 (YB-1)/AR axis in nimotuzumab-induced EMT by overexpressing AR, activating Akt using SC79, and/or downregulating YB-1 using siRNA. Nimotuzumab suppressed the xenograft growth from both LNCaP and PC3 cells in vivo, which was associated with reduced EMT. Consistently, nimotuzumab inhibited proliferation, cell-cycle progression, EMT, and migration/invasion, but stimulated apoptosis of both LNCaP and PC3-AR cells in vitro. On the molecular level, nimotuzumab inactivated Akt and YB-1 and reduced the expression of AR. Boosting AR expression in LNCaP and PC3-AR cells antagonized the action of nimotuzumab, at least partially restored EMT, and enhanced the migration/invasion. We also found that Akt was essential for controlling YB-1 activation, and both critical for regulating the levels of AR and EMT-related biomarkers. In this study, we presented our novel findings that by targeting the Akt/YB-1/AR axis, nimotuzumab significantly inhibited EMT of PC cells. Considering that EMT is a critical mechanism contributing to the metastatic spread of cancer cells, nimotuzumab may become a promising therapy for alleviating the malignant progression of PC. © 2019 IUBMB Life, 1-14, 2019.

2040 related Products with: Nimotuzumab inhibits epithelial-mesenchymal transition in prostate cancer by targeting the Akt/YB-1/AR axis.

Prostate cancer, adjacent Prostate cancer tissue ar Prostate cancer tissue ar Prostate cancer and norma Prostate cancer tissue ar Multiple prostate cancer Prostate cancer tissue ar Prostate cancer tissue ar Prostate cancer, hyperpla Prostate cancer tissue ar Prostate cancer, PIN (pro Prostate cancer and hyper

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Hsp-27 and NF-κB pathway is associated with AR/AR-V7 expression in prostate cancer cells.

In the present study, NF-κB inhibitor BAY 11-7082 and/or Hsp-27 inhibitor KRIBB-3 agents were used to investigate the molecular mechanisms mediating androgen receptor expression on prostate cancer cell lines. The decrease observed in androgen receptor and p65 expressions, particularly at 48 h, in parallel with the decrease in the phosphorylation of the p-IKK α/β and p-Hsp-27 proteins in the LNCaP cells, indicated that androgen receptor inactivation occurred after the inhibition of the NF-κB and Hsp-27. In 22Rv1 cells, androgen receptor variant-7 was also observed to be decreased in the combined dose of 48 h. The association of this decrease with the decrease in androgen receptor and p65 expressions is a supportive result for the role of NF-κB signaling in the formation of androgen receptor variant. In androgen receptor variant-7 siRNA treatment in 22Rv1 cell lines, decrease of expression of androgen receptor variant-7 as well as decrease of expression of androgen receptor and p65 were observed. The decrease statistically significant in androgen receptor and p65 expressions was even greater when siRNA treatment was followed with low dose and time (6 h) combined treatment after transfection. We also showed that increased Noxa and decreased Bcl-2 protein level, indicated that apoptotic induction after this combination. In conclusion, inhibition of NF-κB and Hsp-27 is also important, along with therapies for androgen receptor variant-7 inhibition.

1415 related Products with: Hsp-27 and NF-κB pathway is associated with AR/AR-V7 expression in prostate cancer cells.

JAK pathway ISRE reporter Cancer Apoptosis Phospho- Prostate cancer, adjacent Rabbit Anti-APIP Apaf1 In Rabbit Anti-APIP Apaf1 In anti-Diazepam Binding Inh Prostate cancer tissue ar Prostate cancer tissue ar Prostate cancer and norma Prostate cancer tissue ar Multiple prostate cancer Prostate cancer tissue ar

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Detection of androgen receptor (AR) and AR-V7 in small cell prostate carcinoma: Diagnostic and therapeutic implications.

Small cell prostate carcinoma (SCPC) is a rare and highly malignant subtype of prostate cancer. SCPC frequently lacks androgen receptor (AR) and prostate-specific antigen (PSA) expression, and often responds poorly to androgen deprivation therapy (ADT). AR splice variant-7 (AR-V7) is a truncated AR protein implicated in resistance to AR-targeting therapies. AR-V7 expression in castration-resistant prostate cancers has been evaluated extensively, and blood-based detection of AR-V7 has been associated with lack of response to abiraterone and enzalutamide. However, whether AR-V7 is expressed in SCPC is not known.

2424 related Products with: Detection of androgen receptor (AR) and AR-V7 in small cell prostate carcinoma: Diagnostic and therapeutic implications.

Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 AZD-3514 Mechanisms: Andr Rabbit Anti-Human Androge Goat Anti-Human Androgen Small cell lung carcinoma Non small cell lung carci Non small cell lung carci Lung small cell carcinoma

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Metformin alters H2A.Z dynamics and regulates androgen dependent prostate cancer progression.

Epigenetic mechanisms involved in prostate cancer include hypermethylation of tumor suppressor genes, general hypomethylation of the genome, and alterations in histone posttranslational modifications (PTMs). In addition, over expression of the histone variant H2A.Z as well as deregulated expression of Polycomb group proteins including EZH2 have been well-documented. Recent evidence supports a role for metformin in prostate cancer (PCa) treatment. However, the mechanism of action of metformin in PCa is poorly understood. We provide data showing that metformin epigenetically targets PCa by altering the levels and gene binding dynamics of histone variant H2A.Z. Moreover, we show that the increase in H2A.Z upon metformin treatment occurs preferentially due to H2A.Z.1 isoform. Chromatin immunoprecipitation (ChIP)-RT PCR analysis indicates that metformin treatment results in an increased H2A.Z occupancy on the androgen receptor (AR) and AR-regulated genes that is more prominent in the androgen dependent AR positive LNCaP cells. Repression of H2A.Z.1 gene by siRNA-mediated knock down identified this H2A.Z isoform to be responsible. Based on preliminary data with an EZH2-specific inhibitor, we suggest that the effects of metformin on the early stages of PCa may involve both EZH2 and H2A.Z through the alteration of different molecular pathways.

1333 related Products with: Metformin alters H2A.Z dynamics and regulates androgen dependent prostate cancer progression.

Prostate disease spectrum Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 AZD-3514 Mechanisms: Andr Adrenal gland disease spe Rectum disease spectrum ( Kidney disease spectrum ( Prostate cancer and hyper Prostate cancer, adjacent

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Sarcopenia as a severe organ failure, its diagnosing and present therapeutic possibilities.

Sarcopenia is defined as generalized and progressive age-related loss of skeletal muscle mass, muscle strength and physical performance below a defined threshold. In sarcopenia skeletal muscle mass - the largest body organ - is failing in its function and the term "muscle failure" was suggested. Sarcopeniat is now recognized as a serious clinical problem compromising healthy aging concept and quality of life of affected older people. Sarcopenia has a complex multifactorial pathogenesis, which involves not only age-related changes in neuromuscular function, muscle protein turnover, and hormone levels and sensitivity, but also a chronic pro-inflammatory state, oxidative stress, and behavioral factors - particularly nutritional status and degree of physical activity. The paper provides detailed review of screening and diagnostic methods and consensus-based cut off values and biomarkers of potential patophysiologic mechanisms involved in sarcopenia development in individual patient. Further, detailed description of current preventive and therapeutic strategies for sarcopenia is included. These involve structured physical activities, namely progressive resistance training and aerobic activities which prevent muscle loss and improve muscle performance. The effect of exercise is enhanced by nutritional supplementation, particularly through proteoanabolic effect of proteins and some amino acids. There are no currently registered drugs with indication of sarcopenia but there are promising substances in higher phases of clinical trials (such as antimyostatin human monoclonal antibodies, selective androgen receptor modulators) which have the potential to be introduced into clinical practice soon. Conclusions Sarcopenia is a new clinical diagnosis of organ failure of the skeletal muscle function leading to multiple adverse health outcomes. Physicians should be aware of clinical symptoms and diagnostic algorithm and target treatment according to sarcopenia leading causes. Key words: clinical diagnosis and treatment - muscle failure - muscle mass, strength and function - sarcopenia.

2774 related Products with: Sarcopenia as a severe organ failure, its diagnosing and present therapeutic possibilities.

FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu Normal mouse multiple org Normal rat multiple organ Normal rat multiple organ Normal rat multiple organ Multiple organ cancer tis Multiple organ tumor tiss

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Immunization against Kisspeptin-54 perturb hypothalamic-pituitary-testicular signaling pathway in ram lambs.

Kisspeptin, a peptide product of KISS1 gene, recently identified as essential upstream gatekeeper in hypothalamic-pituitary-gonadal (HPG) axis. This study was designed to investigate the effect of immunization against kisspeptin-54 on hypothalamic-pituitary-testicular signaling pathway. A total of ten intact 56-days-old ram lambs were used and randomized into the treatment and control groups, which were, respectively immunized by kisspeptin-54 based vaccine and the empty plasmid via intramuscular route. We employed indirect enzyme-linked immunosorbent assay and quantitative real-time PCR to characterize the difference in serum kisspeptin, luteinizing hormone, testosterone hormone concentration and mRNA expression of reproductive-related genes in HPG axis across kisspeptin-54 immunized and control ram lambs. Serum kisspeptin, luteinizing hormone and testosterone concentration in the treatment group was lower (p < 0.05) than that of the control group. Compared with the control group, the mRNA expression of the hypothalamic androgen receptor (AR), KISS1, G protein-coupled receptor (GPR54) and gonadotropin-releasing hormone (GnRH) was altered in the immunized group (p < 0.05). Moreover, mRNA expression of pituitary luteinizing hormone beta (LHβ), follicle stimulating hormone beta (FSHβ), and GnRH receptor as well as, testicular LH receptor and FSH receptor, were remarkably lower (P < 0.05) in the treatment group. We concluded that immunization against kisspeptin-54 reduced serum kisspeptin levels thereby, the normal hypothalamic-pituitary-testicular signaling pathway disrupted. This data provides a great insight for the use of kisspeptin to regulate reproduction.

1678 related Products with: Immunization against Kisspeptin-54 perturb hypothalamic-pituitary-testicular signaling pathway in ram lambs.

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