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21.
Won Jeong K Chodankar R Purcell DJ Bittencourt D Stallcup MR 《Molecular endocrinology (Baltimore, Md.)》2012,26(6):955-966
Progesterone receptor (PgR) controls the menstrual cycle, pregnancy, embryonic development, and homeostasis, and it plays important roles in breast cancer development and progression. However, the requirement of coregulators for estrogen-induced expression of the PgR gene has not been fully explored. Here we used RNA interference to demonstrate dramatic differences in requirements of 10 different coregulators for estrogen-regulated expression of six different genes, including PgR and the well-studied TFF1 (or pS2) gene in MCF-7 breast cancer cells. Full estrogen-induced expression of TFF1 required all ten coregulators, but PgR induction required only four of the 10 coregulators. Chromatin immunoprecipitation studies demonstrated several mechanisms responsible for the differential coregulator requirements. Actin-binding coregulator Flightless-I, required for TFF1 expression and recruited to that gene by estrogen receptor-α (ERα), is not required for PgR expression and not recruited to that gene. Protein acetyltransferase tat-interactive protein 60 and ATP-dependent chromatin remodeler Brahma Related Gene 1 are recruited to both genes but are required only for TFF1 expression. Histone methyltransferase G9a is recruited to both genes and required for estrogen-induced expression of TFF1 but negatively regulates estrogen-induced expression of PgR. In contrast, histone methyltransferase myeloid/lymphoid or mixed-lineage leukemia 1 (MLL1), pioneer factor Forkhead box A1, and p160 coregulator steroid receptor coactivator-3 are required for expression of and are recruited to both genes. Depletion of MLL1 decreased ERα binding to the PgR and TFF1 genes. In contrast, depletion of G9a enhanced ERα binding to the PgR gene but had no effect on ERα binding to the TFF1 gene. These studies suggest that differential promoter architecture is responsible for promoter-specific mechanisms of gene regulation. 相似文献
22.
Ianculescu I Wu DY Siegmund KD Stallcup MR 《The Journal of biological chemistry》2012,287(6):4000-4013
23.
NG2 proteoglycan expression in mouse skin: altered postnatal skin development in the NG2 null mouse.
Kuniko Kadoya Jun-Ichi Fukushi Yoshihiro Matsumoto Yu Yamaguchi William B Stallcup 《The journal of histochemistry and cytochemistry》2008,56(3):295-303
In early postnatal mouse skin, the NG2 proteoglycan is expressed in the subcutis, the dermis, the outer root sheath of hair follicles, and the basal keratinocyte layer of the epidermis. With further development, NG2 is most prominently expressed by stem cells in the hair follicle bulge region, as also observed in adult human skin. During telogen and anagen phases of the adult hair cycle, NG2 is also found in stem cell populations that reside in dermal papillae and the outer root sheaths of hair follicles. Ablation of NG2 produces alterations in both the epidermis and subcutis layers of neonatal skin. Compared with wild type, the NG2 null epidermis does not achieve its full thickness due to reduced proliferation of basal keratinocytes that serve as the stem cell population in this layer. Thickening of the subcutis is also delayed in NG2 null skin due to deficiencies in the adipocyte population. 相似文献
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William B. Stallcup 《Brain Cell Biology》2002,31(6-7):423 ppl=-435
The NG2 chondroitin sulfate proteoglycan is a valuable marker for several types of incompletely-differentiated precursor cells, including oligodendrocyte progenitors in the central nervous system, developing mesenchymal cells in cartilage, muscle, and bone, and pericytes/smooth muscle cells in developing vasculature. In addition to extending our knowledge about the developmental roles of these cell types, current studies on NG2 are also providing information about the molecular mechanisms through which the proteoglycan itself influences progenitor development. This research suggests that interaction of NG2 with extracellular and intracellular ligands regulates signaling events that are important for both cell proliferation and cell migration. 相似文献
26.
The intracellular processing of the murine leukemia virus envelope glycoprotein precursor Pr85 to the mature products gp70 and p15e was analyzed in the mouse T-lymphoma cell line W7MG1. Kinetic (pulse-chase) analysis of synthesis and processing, coupled with endoglycosidase (endo H) and neuraminidase digestions revealed the existence of a novel high molecular weight processing intermediate, gp95, containing endo H-resistant terminally glycosylated oligosaccharide chains. In contrast to previously published conclusions, our data indicate that proteolytic cleavage of the envelope precursor occurs after the acquisition of endo H-resistant chains and terminal glycosylation and thus after the mannosidase II step. In the same W7MG1 cell line, the type and order of murine leukemia virus envelope protein processing events was identical to that for the mouse mammary tumor virus envelope protein. Interestingly, complete mouse mammary tumor virus envelope protein processing requires the addition of glucocorticoid hormone, whereas murine leukemia virus envelope protein processing occurs constitutively in these W7MG1 cells. We propose that all retroviral envelope proteins share a common processing pathway in which proteolytic processing is a late event that follows acquisition of endo H resistance and terminal glycosylation. 相似文献
27.
The lysine-183 residues of yeast glyceraldehyde 3-phosphate dehydrogenase, in contrast to the cysteine-149 residues, react independently with acylating and alkylating agents. Modification of all four residues is required to inactivate the enzyme in spite of the fact that this residue is apparently in the neighborhood of the cysteine-149 involved in half-of-the-sites activity. The modification of the lysine-183 residue, however, influences the half-of-the-sites effect since alkylation of the cysteine-149 residues of the enzyme whose lysine-183 residues are acetylated follows a linear pattern with each subunit acting independently. Four lysine residues outside the active site can be modified with fluorodinitrobenzene, causing 80% loss in enzyme activity. Once again each subunit acts independently. This same residue can also be modified by a fluorescein label which can serve as a reporter group for binding and conformational changes occurring at the active site. The results add support for the functional symmetry of the apo-enzyme and demonstrate how the co-operativity between subunits can be altered by amino acid modification. 相似文献
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Estrogen receptor α (ERα) plays critical roles in development and progression of breast cancer. Because ERα activity is strictly dependent upon the interaction with coregulators, coregulators are also believed to contribute to breast tumorigenesis. Cell Cycle and Apoptosis Regulator 1 (CCAR1) is an important co-activator for estrogen-induced gene expression and estrogen-dependent growth of breast cancer cells. Here, we identified Deleted in Breast Cancer 1 (DBC1) as a CCAR1 binding protein. DBC1 was recently shown to function as a negative regulator of the NAD-dependent protein deacetylase SIRT1. DBC1 associates directly with ERα and cooperates synergistically with CCAR1 to enhance ERα function. DBC1 is required for estrogen-induced expression of a subset of ERα target genes as well as breast cancer cell proliferation and for estrogen-induced recruitment of ERα to the target promoters in a gene-specific manner. The mechanism of DBC1 action involves inhibition of SIRT1 interaction with ERα and of SIRT1-mediated deacetylation of ERα. SIRT1 also represses the co-activator synergy between DBC1 and CCAR1 by binding to DBC1 and disrupting its interaction with CCAR1. Our results indicate that DBC1 and SIRT1 play reciprocal roles as major regulators of ERα activity, by regulating DNA binding by ERα and by regulating co-activator synergy. 相似文献
30.