PU.1 Directly Regulates cdk6 Gene Expression, Linking the Cell Proliferation and Differentiation Programs in Erythroid Cells

Choe, Kevin S.; Ujhelly, Olga; Wontakal, Sandeep N.; Skoultchi, Arthur I.

doi:10.1074/jbc.m109.077727

Cited by 29 publications

(32 citation statements)

References 47 publications

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“…Alterations in their levels have been implicated in the pathogenesis of cancer, including both solid and hematopoietic malignancies. These transcriptional factors have been reported to affect all six hallmarks of carcinogenesis through the transcriptional activation of genes associated with cell proliferation, suppression of apoptosis, tumour promotion, metastasis, angiogenesis or invasiveness [68][69][70][71][72]. More recently, NF-κB has been reported to regulate PU.1 through a novel binding site in a 17-kb upstream regulatory element [73].…”

Section: Regulation Of Gene Expressionmentioning

confidence: 96%

Stem cell marker olfactomedin 4: critical appraisal of its characteristics and role in tumorigenesis

Grover

Hardingham

Cummins

2010

Cancer Metastasis Rev

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Olfactomedin 4 (OLFM4), a member of the olfactomedin domain-containing proteins, is a glycoprotein with molecular weight of approximately 64 kDa. The protein is a "robust marker" of Lgr5+ stem cells and has been localised to mitochondria, nuclei and cell membranes. The bulk of OLFM4 exists in a polymeric form which is held together by disulfide bonds and carbohydrate interactions. Earlier studies revealed that the protein binds to lectins and cadherins, and facilitates cell-cell adhesion. Recent data demonstrated that the protein possesses several hallmarks of carcinogenesis. OLFM4 has also been purported to be an inducible resistance factor to apoptotic stimuli such as radiation and anticancer drugs. Here, we review its synonyms and classification, gene structure, protein structure, intracellular and tissue distribution, adhesive and antiapoptotic; mitotic; migratory and cell cycle regulatory characteristics. We also critically evaluate recent advances in understanding of the transcriptional regulation of OLFM4 and its upstream signalling pathways with special emphasis on carcinogenesis and outline future perspectives in the field.

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Section: Regulation Of Gene Expressionmentioning

confidence: 96%

Stem cell marker olfactomedin 4: critical appraisal of its characteristics and role in tumorigenesis

Grover

Hardingham

Cummins

2010

Cancer Metastasis Rev

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“…Phosphorylation of pRb leads to the release of E2F transcription factors and induction of the expression of genes necessary for cell cycle progression. CDK6 was also over-expressed in erythroid cells [48] and in gastric cancer [49]. Otto and Sicinski [50] reported CDK6 can control the formation of blood vessels VEGF-A, which can stimulate the formation of new blood vessels by endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Genome-Wide Microarray Analysis of Long Non-Coding RNAs in Eutopic Secretory Endometrium with Endometriosis

Wang

Yang

et al. 2015

Cell Physiol Biochem

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Background/Aims: Dysregulated long non-coding RNAs (lncRNAs) can lead to the occurrence of various diseases; however, reports of the function of lncRNAs in endometriosis and related studies are scarce. The pathogenesis of endometriosis is still poorly understood. Methods: Dysregulated lncRNAs and mRNAs between eutopic and normal endometrium (both are late secretory) were analyzed by lncRNA microarray. Eight lncRNAs and mRNA CDK6 were validated using quantitative reverse transcription polymerase chain reaction (qRT-PCR). Bioinformatics prediction was used to investigate the potential function of these differentially expressed lncRNAs. Results: Microarray expression profiling suggests 1277 lncRNAs (488 up- and 789 down-regulated) and 1216 mRNAs (578 up- and 638 down-regulated) were expressed differentially between eutopic and normal endometrium. Pathway analysis and gene ontology (GO) analysis found differently expressed lncRNAs associated with the cell cycle and immune regulation. The relative level of expression of CDK6 and AC002454.1 were obtained by qRT-PCR and the Pearson correlation coefficient was 0.747 (p<0.0001). A coding-noncoding gene co-expression (CNC) network was constructed for these validated lncRNAs. Conclusion: These dysregulated lncRNAs might provide information for new biomarkers or novel therapeutic targets of endometriosis. AC002454.1 might induce cell cycle disorder by regulating CDK6 to participate in the pathogenesis of endometriosis.

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“…qChIP was carried out as described in our previous publications (21,(43)(44)(45)(46) with specific modifications described in Sl Materials and Methods. Procedures for protein immunoprecipitation, Western blotting, and protein interactions with GST fusion proteins were described previously (47).…”

Section: Methodsmentioning

confidence: 99%

H1 linker histone promotes epigenetic silencing by regulating both DNA methylation and histone H3 methylation

Yang

Kim

Toro

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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106

105

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Epigenetic silencing in mammals involves DNA methylation and posttranslational modifications of core histones. Here we show that the H1 linker histone plays a key role in regulating both DNA methylation and histone H3 methylation at the H19 and Gtl2 loci in mouse ES cells. Some, but not all, murine H1 subtypes interact with DNA methyltransferases DNMT1 and DNMT3B. The interactions are direct and require a portion of the H1 C-terminal domain. Expression of an H1 subtype that interacts with DNMT1 and DNMT3B in ES cells leads to their recruitment and DNA methylation of the H19 and Gtl2 imprinting control regions. H1 also interferes with binding of the SET7/9 histone methyltransferase to the imprinting control regions, inhibiting production of an activating methylation mark on histone H3 lysine 4. H1-dependent recruitment of DNMT1 and DNMT3B and interference with the binding of SET7/9 also were observed with chromatin reconstituted in vitro. The data support a model in which H1 plays an active role in helping direct two processes that lead to the formation of epigenetic silencing marks. The data also provide evidence for functional differences among the H1 subtypes expressed in somatic mammalian cells.mouse embryonic stem cell | H1 histone triple knockout T wo major types of epigenetic marks occur in mammalian genomes, DNA methylation and posttranslational modifications of histones (1, 2). The methylation of cytosines in mammalian DNA occurs primarily at CpG dinucleotides and is essential for normal mammalian development (1, 3). Perturbations of DNA methylation patterns are thought to play a role in cancer development (4). There are two classes of mammalian DNA methyltransferases (DNMTs), one that functions primarily to establish DNA methylation de novo (DNMT3A and DNMT3B) and the other to maintain it (DNMT1) (3). DNA methylation can have profound effects on gene expression and is most often associated with transcriptional silencing (1, 2). Accumulating evidence indicates the existence of crosstalk between the DNA methylation and core histone modification systems (1, 2). For example, mouse ES cells deficient for the histone H3 lysine 9 (H3K9) methyltransferases Suv39h1/h2 exhibit hypomethylation of CpGs at a subset of repetitive DNA elements (5). Additionally, several lines of evidence indicate that the presence of unmethylated lysine 4 of histone H3 (H3K4) in chromatin favors de novo methylation of DNA (6-9). Despite these advances, the factors in chromatin that coordinate DNA methylation and histone H3 methylation have not been identified.In this study, we investigated the role of the linker histone H1 in regulating DNA methylation and histone H3 methylation at the H19 and Gtl2 loci in mouse ES cells. H1 is the most distinct of the five histone proteins (H1, H2A, H2B, H3, and H4) in chromatin (10,11). Mammals contain at least eight histone H1 subtypes or variants that differ in amino acid sequences and expression during development (12-14). Functional differences among these subtypes have been difficult to identif...

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PU.1 Directly Regulates cdk6 Gene Expression, Linking the Cell Proliferation and Differentiation Programs in Erythroid Cells

Cited by 29 publications

References 47 publications

Stem cell marker olfactomedin 4: critical appraisal of its characteristics and role in tumorigenesis

Stem cell marker olfactomedin 4: critical appraisal of its characteristics and role in tumorigenesis

Genome-Wide Microarray Analysis of Long Non-Coding RNAs in Eutopic Secretory Endometrium with Endometriosis

H1 linker histone promotes epigenetic silencing by regulating both DNA methylation and histone H3 methylation

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