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Egf Regulation Of Nuclear Co Activator Aib1 Function In Breast Cancer
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Book Synopsis EGF Regulation of Nuclear Co-Activator AIB1 Function in Breast Cancer by :
Download or read book EGF Regulation of Nuclear Co-Activator AIB1 Function in Breast Cancer written by and published by . This book was released on 2002 with total page 16 pages. Available in PDF, EPUB and Kindle. Book excerpt: Various growth factor receptor pathways promote human breast tumorigenesis of hormone-independent tumors. The nuclear receptor coactivator AIBi (amplified in breast cancer 1) can be phosphorylated and regulated by growth factor-induced signaling pathways such as MAP kinase and IkB kinase. Our lab has found a splice variant of AIBl, called delta exon3 AIBl, which has a higher co-activating ability than the full-length protein. This study determined the ability of delta exon3 splice variant compared with AIBi in potentiating growth factor signaling and to determine the mechanism of this potentiation using a growth factor responsive promoter.
Book Synopsis Regulation and Role of Nuclear Receptor Coactivator AIB1 in Breast Cancer by :
Download or read book Regulation and Role of Nuclear Receptor Coactivator AIB1 in Breast Cancer written by and published by . This book was released on 2002 with total page 51 pages. Available in PDF, EPUB and Kindle. Book excerpt: AIB1 (Amplified In Breast cancer 1) is a nuclear receptor coactivator found amplified and overexpressed in a subset of breast cancers. AIBl potentiates the transcriptional activity of the estrogen, progesterone, thyroid hormone, and retinoid receptors. It is necessary for normal female reproductive function and mammary gland development and is rate-limiting for tumor growth in nude mice. It is hypothesized that the amplification and overexpression of AIBl contribute to the promotion and/or progression of breast cancer. An understanding of the regulation of expression of AIB1 will give insight into the role of AIB1 in breast cancer. This work has shown that antiestrogens, retinoids, and TGF-beta contribute to the overexpression of AIB1 in MCK-7 breast cancer cells. The putative promoter for the AIB1 gene has been identified. Regulatory elements involved in the regulation of AIB1 by antiestrogens, retinoids, and TGF-beta were not found in the cloned promoter regions and may be upstream or intronic enhancer elements. Further studies will explore the consequences of overexpression of AIB1 through stable transfection into a cell line with low endogenous levels of AIB1.
Book Synopsis The Role of Nuclear Receptor Coactivator A1B1 in Growth Factor-Mediated Mammary Tumorigenesis by :
Download or read book The Role of Nuclear Receptor Coactivator A1B1 in Growth Factor-Mediated Mammary Tumorigenesis written by and published by . This book was released on 2008 with total page 13 pages. Available in PDF, EPUB and Kindle. Book excerpt: AIBI (Amplified In Breast Cancer I) is a nuclear receptor coactivator whose gene is amplified in 5-10% of breast cancers and both the mRNA and protein are overexpressed in 30% of breast tumors. In vitro studies show that AIBI plays a significant role in estrogen and IGF-1-induced cell proliferation. Germline knockout of the AIBI gene leads to reduced somatic growth abnormal reproductive function and reduced mammary gland development. Knockout of AIBI expression also abrogates Ras-induced tumorigenesis. Furthermore patients with tumors expressing high levels of the growth factor HER2/Neu in addition to AIBI often develop anti-estrogen resistance to tamoxifen therapy. These findings imply that AIBI plays a fundamental role in the development of hormone-independent breast cancer through growth factor mediated pathways. Nonetheless the underlying mechanism of AIBI regulation of growth factor mediated mammary neoplasia is unknown. In this invesbgation I will utilize the MMTV-Neu mouse model (develop mammary gland tumors in 7-9 months) to elucidate the specific role of AIBI in growth factor-induced mammary tumorigenesis.
Book Synopsis Regulation of the Activity of AIB1, an Estrogen Coactivator, by Growth Factor Signals by :
Download or read book Regulation of the Activity of AIB1, an Estrogen Coactivator, by Growth Factor Signals written by and published by . This book was released on 2002 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: AIB1 is a member of a coactivator family that potentiates the transcriptional activity of nuclear hormone receptors. The AIB1 gene is amplified in certain breast and ovarian cancers. AIB1 amplification is preferentially found in ER and progesterone receptor-positive breast cancers. These findings suggest that AIB1 plays a causative role in breast cancer development. Our lab recently identified AIB1 as a target of the MAPK signaling pathway (Font de Mora and Brown, Mol Cell Biol 20:5041, 2000). This signaling pathway is triggered by growth factors of the insulin-like growth factor (IGF) and epidermal growth factor (EGF) family. These growth factors and their receptors have also been implicated in the development and progression of breast tumors. Based on these findings, we propose that the phosphorylation of AIB1 by MAPK may represent part of the molecular mechanism that integrates signals from steroid hormones and growth factors. Furthermore, we hypothesize that AIB1 phosphorylation may contribute to the role that AIB1 plays in the development of breast cancer. In order to identify the sites of AIB1 that are phosphorylated by MAPK, seven potential MAPK phosphorylation sites were targeted for deletion and mutations. In vitro phosphorylation of the point mutations and internal deletions by Erk2 revealed 4 major sites of phosphorylation. In the future we plan to test these mutants for their ability to function as coactivators. Our study will help to understand how AIB1 activity is modulated by MAPK. This may help to determine how AIB1 is involved in the development of breast cancer.
Book Synopsis Targeting of the Nuclear Receptor Coactivator Isoform DELTA3AIB1 in Breast Cancer by :
Download or read book Targeting of the Nuclear Receptor Coactivator Isoform DELTA3AIB1 in Breast Cancer written by and published by . This book was released on 2007 with total page 19 pages. Available in PDF, EPUB and Kindle. Book excerpt: AIB1 which stands for Amplified in Breast Cancer, codes for a protein that is a member of the steroid receptor coactivator (SRC) family. AIB1 is amplified in approximately 5-10% of breast cancers and the mRNA and protein overexpressed in>30% of breast cancers. AIB1 interacts with a superfamily of ligand activated nuclear receptors to potentiate transcriptional activity leading to upregulation of downstream target gene expression. An important finding was that an isoform of AIB1 (Delta3AIB1) is a significantly more effective coactivator of the estrogen receptor than AIB1 and is highly overexpressed in human breast cancer. Prior work in our lab showed that the downregulation of overall levels of AIB1 plus DELTA3AIB1, using a regulatable AIB1 directed ribozyme, resulted in reduced tumor growth in vivo. Overall, these data indicate a major role for AIB1 and its isoform DELTA3AIB1 in breast cancer development and growth. However the relative roles of AIB1 versus the more highly active DELTA3AIB1 in phenotypic changes in the breast has not been determined. In this investigation, we are developing a method to use siRNA directed at DELTA3AIB1 in order investigate its role in breast cancer and as a possible future therapeutic approach to breast cancer.
Book Synopsis Placat angaaende Oprettelsen af en Direction for Universitetet og de lærde Skoler i Danmark og Norge by :
Download or read book Placat angaaende Oprettelsen af en Direction for Universitetet og de lærde Skoler i Danmark og Norge written by and published by . This book was released on 1950 with total page 2 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Book Synopsis Regulation of the Activity of AIB1 an Estrogen Receptor Coactivator by Growth Factor Signals by :
Download or read book Regulation of the Activity of AIB1 an Estrogen Receptor Coactivator by Growth Factor Signals written by and published by . This book was released on 2003 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: The AIB1 protein is a member of a coactivator family that potentiates the transcriptional activity of the nuclear hormone receptors. AIB1, is amplified in certain breast and ovarian cancers and has been suggested that AIB1 plays a causative role in breast cancer development. Our lab recently identified AIB1 as a target of the MAPK signaling pathway (Font de Mora and Brown, Mol Cell Biol 20:5041, 2000). Based on these findings, we propose that the phosphorylation of AIB1 by MAPK may represent part of the molecular mechanism that integrates signals from steroid hormones and growth factors. In order to identify the sites of AIB1 that are phosphorylated by MAPK, seven potential phosphorylation sites were targeted for point mutations and or deletions. Previously we showed by an In vitro phosphorylation assay by (Erk2) that three out of the seven putative phosphorylation sites tested were most likely to be the specific MAPK phosphorylation sites. In order to investigate the physiological relevance of the AIB1 phosphorylation sites, we subcloned all mutants into GAL4DBD vector. We found that those mutants that showed low phosphorytation in vitro, gave the lowest transactivation levels when tested in vivo. In addition we were able to differentiate the sub-cellular localization of AIB1 after phosphorylation by performing transient transfection in COS cells using a constitutively active MAPK vector and a kinase inhibitor vector and further on performing immunofluorescence.
Book Synopsis Role of a Novel Splice Variant of the Steroid Receptor Coactivator AIB1 in Breast Cancer by :
Download or read book Role of a Novel Splice Variant of the Steroid Receptor Coactivator AIB1 in Breast Cancer written by and published by . This book was released on 2004 with total page 24 pages. Available in PDF, EPUB and Kindle. Book excerpt: In this proposal we have investigated the hypothesis that overexpression of a novel truncated version of AIBl (Delta3AIBl) that we have found to be overexpressed in breast cancer is important for tumor development by impacting upon nuclear hormone receptor function. We have examined the hypothesis that the novel AIBl variant has an altered function that changes its interaction with nuclear receptors such as the estrogen or progesterone receptor. We propose that changes in the level of expression of the novel AIBl variant will support tumor progression and may well have prognostic significance for breast cancer. We have now determined that Delta3AIBl is overexpressed relative to the full-length protein in breast cancer tumor samples and cell lines. We have also determined that Delta3AIBl is a significantly more active coactivator that full-length AIBl on the estrogen and progesterone receptor (J. Biol. Chem. 276, 39736-39741, 2001). Delta3AIBl also plays a role in tamoxifen resistance and its overexpression makes tamoxifen a much more potent estrogen (Oncogene 23, 403-409, 2004). In addition, a surprising finding is that overexpression of Delta3AIBl can also potentiate EGF signaling. This implies that Delta3AIB1 can also drive hormone and non-hormone mediated proliferation in breast cancer.
Book Synopsis The Role of Nuclear Receptor Coactivator Aib1/src3 in Normal and Breast Cancer Stromal Functions by : Maram Abdulmohsen Al-Otaiby
Download or read book The Role of Nuclear Receptor Coactivator Aib1/src3 in Normal and Breast Cancer Stromal Functions written by Maram Abdulmohsen Al-Otaiby and published by . This book was released on 2012 with total page 332 pages. Available in PDF, EPUB and Kindle. Book excerpt: The nuclear receptor coactivator amplified in breast cancer 1 (AIB1/SRC3) has a well-defined role in steroid and growth factor signaling in cancer and normal epithelial cells. Less is known about its function in stromal cells, though AIB1/SRC3 is upregulated in tumor stroma and may thus contribute to tumor angiogenesis. In addition, our lab has demonstrated previously a potential impact of AIB1/SRC3 on tumor stroma as reduced angiogenesis was observed in mammary tumors in AIB1/SRC3 knockout mice. In this study, we report for the first time the effect of AIB1/SRC3 on the function of two types of stromal cells and on keratinocytes in vitro. Endothelial cell functions including formation of tube like structures, monolayer formation, migration, proliferation and apoptosis were all inhibited by reduction in AIB1. We also observed reduction on FGF2-induced signaling of endothelial cells in vitro when AIB1/SRC3 levels were reduced. Moreover, AIB1/SRC3 did not impact fibroblast proliferation, but did impact its migration. We also observed that AIB1/SRC3 had a significant effect on keratinocyte proliferation through the up regulation of a number of cell cycle molecules. In AIB1/SRC3+/- and AIB1/SRC3-/- mice, the angiogenic responses to subcutaneous Matrigel implants were reduced by two thirds and exogenously added FGF2 did not overcome this deficiency. Furthermore, AIB1/SRC3+/- and AIB1/SRC3-/- mice showed a similarly delayed healing of full-thickness excisional skin wounds indicating that both alleles were required for proper tissue repair. Analysis of this defective wound healing showed reduced recruitment of inflammatory cells and macrophages, cytokine induction and metalloprotease activity. Skin grafts from animals with different AIB1 genotype and subsequent wounding of the grafts revealed that the defective healing is attributable to local factors and not to defective bone marrow responses. Indeed, wounds in AIB1/SRC3+/- mice showed reduced expression of FGF10, FGFBP3, FGFR1, FGFR2b and FGFR3, major local drivers of angiogenesis. Further, we examined the influence of AIB1/SRC3 in the epithelial and stromal cross talk in breast cancer. We reported that AIB1/SRC3 has a critical role in the stromal compartment during mammary tumor development. The loss of one allele of AIB1/SRC3 in the stroma significantly delayed tumorigenesis.
Book Synopsis Role of Nuclear Receptor Coactivators, AIB-1 and SRC-1, in the Development of Breast Cancer by :
Download or read book Role of Nuclear Receptor Coactivators, AIB-1 and SRC-1, in the Development of Breast Cancer written by and published by . This book was released on 2000 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: Steroid hormones are involved in the development and growth of the breast cancer. Drugs which inhibit estrogen action are commonly used to inhibit breast cancer growth. Unfortunately, most advanced breast cancer become resistant to estrogen treatment. Recently, many steroid receptor coactivators have been discovered and found to potentiate the transcriptional activity of steroid receptors and enhance the expression of hormone response genes. SRC-1 family of coactivator, AIB1 is found amplified and/or over-expressed in breast cancer specimens. To evaluate the potential roles of SRC-1 family of coactivators in mammary tumorigenesis in vivo, we proposed to generated transgenic mice over-expression of AIB1 (SRC-3) in mammary glands. To target the expression of AIB1 1 in mammary gland, we placed the AIB1 1 transgene under the control of the MMTV-LTR promoter. Two lines of transgenic mice expressing AIB1 1 have been generated. Studies on these transgenic mice will help understanding the development and progression of breast cancer and provide molecular basis for design novel strategies to curb and ultimately cure breast cancer.
Book Synopsis TRANSCRIPTIONAL REPRESSION OF THE NUCLEAR RECEPTOR COACTIVATOR AIB1 BY FOXG1 LEADS TO APOPTOSIS IN BREAST CANCER CELLS by : Jordan V. Li
Download or read book TRANSCRIPTIONAL REPRESSION OF THE NUCLEAR RECEPTOR COACTIVATOR AIB1 BY FOXG1 LEADS TO APOPTOSIS IN BREAST CANCER CELLS written by Jordan V. Li and published by . This book was released on 2013 with total page 260 pages. Available in PDF, EPUB and Kindle. Book excerpt: The oncogene nuclear receptor coactivator amplified in breast cancer 1 (AIB1) is a transcriptional coactivator that is overexpressed in various types of human cancers. However, the molecular mechanisms controlling AIB1 expression in the majority of cancers remain unclear. In this study, we identified a novel interacting protein of AIB1, forkhead-box protein G1 (FoxG1), which is an evolutionarily-conserved forkhead-box transcriptional corepressor. We show that FoxG1 expression is low in breast cancer cell lines, and that low levels of FoxG1 are correlated with a worse prognosis in breast cancer. We also demonstrate that transient overexpression of FoxG1 can suppress endogenous levels of AIB1 mRNA and protein in MCF-7 breast cancer cells. Exogenously expressed FoxG1 in MCF-7 cells also leads to apoptosis that can be rescued in part by AIB1 overexpression. Using chromatin immunoprecipitation (ChIP), we determined that FoxG1 is recruited to a region of the AIB1 gene promoter previously characterized to be responsible for AIB1-induced, positive auto-regulation of transcription through the recruitment of an activating, multiprotein complex, involving AIB1, E2F1 and Sp1. Increased FoxG1 expression significantly reduces the recruitment of AIB1, E2F1 and p300 to this region of the endogenous AIB1 gene promoter. Our data imply that FoxG1 can function as a pro-apoptotic factor in part through suppression of AIB1 coactivator transcription complex formation, thereby reducing the expression of the AIB1 oncogene.
Book Synopsis Isolation and Characterization of AIB1 by : Sarah Lynn Anzick
Download or read book Isolation and Characterization of AIB1 written by Sarah Lynn Anzick and published by . This book was released on 2000 with total page 370 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Book Synopsis Targeting of the Nuclear Receptor Coactivator Isoform Delta3Air in Breast Cancer by :
Download or read book Targeting of the Nuclear Receptor Coactivator Isoform Delta3Air in Breast Cancer written by and published by . This book was released on 2005 with total page 21 pages. Available in PDF, EPUB and Kindle. Book excerpt: Of particular interest to breast cancer was the discovery that an area of chromosome 20q, known to be frequently amplified in breast cancer, harbored the gene for AIB1. AIB1 which stands for "Amplified in Breast cancer" codes for a protein which is a member of the steroid receptor coactivator (SRC) family. AIB1 is amplified in approximately 5-10% of breast cancers and the mRNA and protein overexpressed in>30% of breast cancers. AIB1 interacts with a superfamily of ligand activated nuclear receptors including the estrogen receptor (ER) and progesterone receptor (PR) to potentiate transcriptional activity leading to upregulation of downstream target gene expression. An important finding was that an isoform of AIB1 (delta3AIB1) is a significantly more effective coactivator of the estrogen receptor than AIB1 and is highly overexpressed in human breast cancer. Prior work in our lab showed that the downregulation of overall levels of AIB1 plus delta3AIB1, using a regulatable AIB1 directed ribozyme, resulted in reduced tumor growth in vivo. Overall, these data indicate a major role for AIB1 and its isoform delta3AIB1 in breast cancer development and growth. However the relative roles of AIB1 versus the more highly active delta3AIB1 in phenotypic changes in the breast has not been determined.
Book Synopsis Targeting of the Nuclear Receptor Coativator Isoform Delta 3aib1 in Breast Cancer. Addendum by :
Download or read book Targeting of the Nuclear Receptor Coativator Isoform Delta 3aib1 in Breast Cancer. Addendum written by and published by . This book was released on 2007 with total page 12 pages. Available in PDF, EPUB and Kindle. Book excerpt: AIB1 which stands for "Amplified in Breast Cancer" codes for a protein that is a member of the steroid receptor coactivator (SRC) family. AIB1 is amplified in approximately 5-10% of breast cancers and the mRNA and protein overexpressed in>30% of breast cancers. AIB1 interacts with a super family of ligand activated nuclear receptors to potentiate transcriptional activity leading to upregulation of downstream target gene expression. An important finding was that an isoform of AIB1 (DELTA 3AIB1) is a significantly more effective coactivator of the estrogen receptor than AIB1 and is highly overexpressed in human breast cancer. Prior work in our lab showed that the downregulation of overall levels of AIB1 plus DELTA 3AIB1, using a regulatable AIB1 directed ribozyme, resulted in reduced tumor growth in vivo. Overall, these data indicate a major role for AIB1 and its isoform DELTA 3AIB1 in breast cancer development and growth. However the relative roles of AIB1 versus the more highly active DELTA 3AIB1 in phenotypic changes in the breast has not been determined. In this investigation, we are developing a method to use siRNA directed at DELTA 3AIB1 in order investigate its role in breast cancer and as a possible future therapeutic approach to breast cancer.
Book Synopsis The Nuclear Receptor Co-Activator 5 is a Potential New Co-regulator of the Estrogen Related Receptor [alpha] in Breast Cancer by : Amandine Laffitte
Download or read book The Nuclear Receptor Co-Activator 5 is a Potential New Co-regulator of the Estrogen Related Receptor [alpha] in Breast Cancer written by Amandine Laffitte and published by . This book was released on 2017 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: "Nuclear receptors are transcriptional factors that are essential for a wide range of biological processes. They are partly regulated through their interaction with co-regulatory proteins. Here, we focus on the orphan nuclear receptor ERRa and its potential new co-activator protein NCOA5. Using NCOA5 knockdown or overexpression via a lentiviral system, we investigated the role of NCOA5 in ERRa regulation in Her2-positive breast cancer cells and its effect on known targets of ERRa in this context, such as the ERBB2 amplicon transcription. We show that NCOA5 and ERRa can regulate each other, yet the precise mechanism remains to be elucidated. NCOA5 protein level affects ERR[alpha] transcription and protein level, also affecting the transcription of ERRa targets from the ERBB2 amplicon including the Her2 receptor itself. Modulation of NCOA5 levels leads to variation in cell proliferation and metabolism, thus revealing that NCOA5 is an important factor in the ERBB2 amplicon regulation." --
Book Synopsis Expression Levels of the Nuclear Coactivator AIB1 in Drug Resistance and Tumor Progression of Triple Negative Breast Cancer by : Francisco Rodolfo Saenz
Download or read book Expression Levels of the Nuclear Coactivator AIB1 in Drug Resistance and Tumor Progression of Triple Negative Breast Cancer written by Francisco Rodolfo Saenz and published by . This book was released on 2019 with total page 302 pages. Available in PDF, EPUB and Kindle. Book excerpt: Breast cancer is the most diagnosed cancer and the most frequent cause of cancer mortality in women worldwide. Immunoreactive assays as well as gene expression profiling of breast cancer have shown a high degree of heterogeneity resulting in subtypes with prognostic value for treatment response. The triple negative breast cancer (TNBC) subtype lacks the expression of hormone receptors (ER/PR) and the amplification of HER2 but it expresses basal keratin markers. TNBC represents 15-20% of all invasive breast cancer cases in the United States (US). Clinical, molecular, and genetic characteristics of TNBC include early-onset, aggressive phenotype, higher histological grade, and poor outcome. Attributable risk factors associated with TNBC include reproductive stage and age, race, and genetic factors. Disproportional mortality rates in TNBC affect premenopausal women of African ancestry compared to women of European ancestry. The nuclear receptor coactivator Amplified in Breast Cancer 1 (AIB1) plays a major role in the progression of hormone- and HER2-dependent breast cancers. Here, we examined AIB1's role in TNBC. We determined that acute depletion of AIB1 by shRNA significantly reduces cell survival in basal-like (BL) and mesenchymal (M) TNBC cell lines. Surviving cells with reduced AIB1 (AIB1LOW) can be maintained with stably low mRNA and protein levels of AIB1 in vitro and as xenografts in vivo. (BL2) HCC1806 AIB1LOW cells proliferate independent of serum supplementation and show delayed adhesion kinetics to cell culture dishes. Also, AIB1LOW cells from (BL2) and (M) subtypes of TNBC show a significant reduced tube-formation phenotype when cultured on a basement membrane. Similarly, chemotherapy treatments using (BL2) HCC1806 cell line also resulted in a surviving AIB1LOW population with decreased tube-formation capacity. Gene expression analysis of (BL2) HCC1806 AIB1LOW cell lines revealed a significant enrichment in pro-inflammatory pathways in vitro. Orthotopic injections using limiting dilutions of (BL2) HCC1806 AIB1LOW resulted in smaller size tumors and reduced incidence of pulmonary metastases in immunocompromised mice. Transcriptomic analysis of xenograft tissues revealed that (BL2) HCC1806 AIB1LOW tumor cells had significantly reduced expression in tissue remodeling related genes. Overall, our data suggest that therapeutic interventions such as chemotherapy induces reduction of AIB1 protein in surviving TNBC cell lines in vitro. Chemotherapy-induced AIB1LOW TNBC cells may represent a model of therapy resistance often associated to dormant cells contributing to recurrence or metastasis in TNBC.
Book Synopsis Regulatory Mechanisms in Transcriptional Signaling by :
Download or read book Regulatory Mechanisms in Transcriptional Signaling written by and published by Academic Press. This book was released on 2009-07-25 with total page 413 pages. Available in PDF, EPUB and Kindle. Book excerpt: Regulatory Mechanisms in Transcriptional Signaling, volume of Progress in Molecular Biology and Translational Science, includes in-depth discussion on roles of Chromatin remodeling proteins in nuclear receptor signaling, and the ANCCA regulator in cancer. This important resource, edited by Dr. Debabrata (Debu) Chakravarti, offers research on the progesterone receptor action in leiomyoma and endometrial cancer and emerging roles of the ubiquitin protein system in nuclear hormone receptor signaling to provide the reader with expert discussions of up-to-date research.
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