Developmental expression profiles and distinct regional estrogen responsiveness suggest a novel role for the steroid receptor coactivator SRC‐1 as a discriminative amplifier of estrogen signaling in the rat brain

2003 ◽  
Vol 17 (3) ◽  
pp. 1-12 ◽  
Author(s):  
Yuri A. Mitev ◽  
Siegmund S. Wolf ◽  
Osborne F.X. Almeida ◽  
Vladimir K. Patchev
Keyword(s):  
Rat Brain ◽  
Expression Profiles ◽  
Steroid Receptor ◽  
Developmental Expression ◽  
Estrogen Signaling ◽  
Steroid Receptor Coactivator

scholarly journals Glucocorticoids Do Not Alter Developmental Expression of Hippocampal or Pituitary Steroid Receptor Coactivator-1 and -2 in the Late Gestation Fetal Guinea Pig

Endocrinology ◽  
2004 ◽  
Vol 145 (8) ◽  
pp. 3796-3803 ◽  
Author(s):  
Elaine Setiawan ◽  
Dawn Owen ◽  
Lucy McCabe ◽  
Alice Kostaki ◽  
Marcus H. Andrews ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Steroid Receptor ◽  
Late Gestation ◽  
Developmental Expression ◽  
Steroid Receptor Coactivator

scholarly journals Estrogen-Regulated Prohibitin Is Required for Mouse Uterine Development and Adult Function

Endocrinology ◽  
2011 ◽  
Vol 152 (3) ◽  
pp. 1047-1056 ◽  
Author(s):  
Bin He ◽  
Tae Hoon Kim ◽  
Ramakrishna Kommagani ◽  
Qin Feng ◽  
Rainer B. Lanz ◽  
...  
Keyword(s):  
Target Genes ◽  
Cultured Cells ◽  
Physiological Role ◽  
Reproductive Function ◽  
Steroid Receptor ◽  
Estrogen Signaling ◽  
Steroid Receptor Coactivator ◽  
Regulated Gene Expression ◽  
Uterine Development

Estrogen signaling is pivotal for maintenance of female reproductive function in mammals. The physiological role of estrogen is mediated by estrogen receptors (ERs) and the steroid receptor coactivator family of transcriptional coregulators. Ablation of steroid receptor coactivator and ER coactivators in mice causes impaired female reproductive function. Recently we reported that prohibitin (PHB) can function as a corepressor for ERs in cultured cells. In this study, we demonstrate that PHB is an estrogen-regulated gene in vitro and in vivo, and its expression is induced by estrogen in the uterus, suggesting the existence of feedback regulatory loops. A conditional PHB knockout mouse model was generated by gene targeting to assess its in vivo function. Female mice with selective ablation of the PHB allele in the uterus were sterile, and their uteri were severely hypoplastic, indicating PHB is required for uterine development. Moreover, expression of ER and progesterone receptor target genes was selectively altered in response to hormone treatment. In summary, this study demonstrates that PHB is an estrogen-regulated gene and that PHB is essential for mouse uterine development and adult function and selectively required for estrogen-regulated gene expression.

Molecular Basis for Cold-Intolerant Yang-Deficient Constitution of Traditional Chinese Medicine

2008 ◽  
Vol 36 (05) ◽  
pp. 827-834 ◽  
Author(s):  
Qi Wang ◽  
Shilin Yao
Keyword(s):  
Gene Expression ◽  
Chinese Medicine ◽  
Traditional Chinese Medicine ◽  
Thyroid Hormone Receptor ◽  
Binding Protein ◽  
Expression Profiles ◽  
White Blood Cells ◽  
Steroid Receptor ◽  
Biochemical Basis ◽  
Steroid Receptor Coactivator

Based on the theory of constitution of Traditional Chinese Medicine (TCM), the human population can be classified into nine constitutions including a balanced constitution and eight unbalanced constitutions (Yang-deficient, Yin-deficient, Qi-deficient, Phlegm-wetness, Wetness-heat, Stagnant blood, Depressed, and Inherited special constitutions). Generally, unbalanced constitutions are more susceptible to certain diseases than balanced constitutions. However, whether such constitution classification has modern genetic and biochemical basis is poorly understood. Here we examined gene expression profiles in peripheral white blood cells from eight individuals with Yang-deficient constitutions and six individuals with balanced constitutions using Affymetrix U133 plus 2.0 expression array. Based on a q < 0.05 and fold-change ≥ 2 cutoff, we have identified that 785 genes are up-regulated and 954 genes are down-regulated in Yang-deficient constitution compared to a balanced constitution. Importantly, we found that the expression of thyroid hormone receptor beta (TRβ) and several key nuclear receptor coactivators including steroid receptor coactivator 1 (SRC1), steroid receptor coactivator 3 (SRC3), cAMP-response element-binding protein (CREB) binding protein (CBP) and Mediator is significantly decreased. Such decreased expression of TR transcription complex may lead to impaired thermogenesis, providing a molecular explanation of the main symptom associated with Yang-deficient constitution, cold intolerance. Future studies are needed to validate these gene expression changes in additional populations and address the underlying mechanisms for differential gene expression.

scholarly journals Early and late stage MPN patients show distinct gene expression profiles in CD34+ cells

2021 ◽  
Author(s):  
Julian Baumeister ◽  
Tiago Maié ◽  
Nicolas Chatain ◽  
Lin Gan ◽  
Barbora Weinbergerova ◽  
...  
Keyword(s):  
Gene Expression ◽  
Late Stage ◽  
Rna Splicing ◽  
Bone Marrow Cells ◽  
Myeloproliferative Neoplasms ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Primary Myelofibrosis ◽  
Estrogen Signaling ◽  
Therapeutic Modalities

AbstractMyeloproliferative neoplasms (MPN), comprising essential thrombocythemia (ET), polycythemia vera (PV), and primary myelofibrosis (PMF), are hematological disorders of the myeloid lineage characterized by hyperproliferation of mature blood cells. The prediction of the clinical course and progression remains difficult and new therapeutic modalities are required. We conducted a CD34+ gene expression study to identify signatures and potential biomarkers in the different MPN subtypes with the aim to improve treatment and prevent the transformation from the rather benign chronic state to a more malignant aggressive state. We report here on a systematic gene expression analysis (GEA) of CD34+ peripheral blood or bone marrow cells derived from 30 patients with MPN including all subtypes (ET (n = 6), PV (n = 11), PMF (n = 9), secondary MF (SMF; post-ET-/post-PV-MF; n = 4)) and six healthy donors. GEA revealed a variety of differentially regulated genes in the different MPN subtypes vs. controls, with a higher number in PMF/SMF (200/272 genes) than in ET/PV (132/121). PROGENγ analysis revealed significant induction of TNFα/NF-κB signaling (particularly in SMF) and reduction of estrogen signaling (PMF and SMF). Consistently, inflammatory GO terms were enriched in PMF/SMF, whereas RNA splicing–associated biological processes were downregulated in PMF. Differentially regulated genes that might be utilized as diagnostic/prognostic markers were identified, such as AREG, CYBB, DNTT, TIMD4, VCAM1, and S100 family members (S100A4/8/9/10/12). Additionally, 98 genes (including CLEC1B, CMTM5, CXCL8, DACH1, and RADX) were deregulated solely in SMF and may be used to predict progression from early to late stage MPN. Graphical abstract

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