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Articles 1 - 5 of 5

Full-Text Articles in Cell Biology

Aurkb-Mediated Effects On Chromatin Regulate Binding Versus Release Of Xist Rna To The Inactive Chromosome, Lisa L. Hall, Meg Byron, Gayle Jeannette Pageau, Jeanne B. Lawrence Aug 2009

Aurkb-Mediated Effects On Chromatin Regulate Binding Versus Release Of Xist Rna To The Inactive Chromosome, Lisa L. Hall, Meg Byron, Gayle Jeannette Pageau, Jeanne B. Lawrence

Open Access Articles

How XIST RNA strictly localizes across the inactive X chromosome is unknown; however, prophase release of human XIST RNA provides a clue. Tests of inhibitors that mimic mitotic chromatin modifications implicated an indirect role of PP1 (protein phosphatase 1), potentially via its interphase repression of Aurora B kinase (AURKB), which phosphorylates H3 and chromosomal proteins at prophase. RNA interference to AURKB causes mitotic retention of XIST RNA, unlike other mitotic or broad kinase inhibitors. Thus, AURKB plays an unexpected role in regulating RNA binding to heterochromatin, independent of mechanics of mitosis. H3 phosphorylation (H3ph) was shown to precede XIST RNA ...


Signal Transduction Cross Talk Mediated By Jun N-Terminal Kinase-Interacting Protein And Insulin Receptor Substrate Scaffold Protein Complexes, Claire L. Standen, Norman J. Kennedy, Richard A. Flavell, Roger J. Davis Jul 2009

Signal Transduction Cross Talk Mediated By Jun N-Terminal Kinase-Interacting Protein And Insulin Receptor Substrate Scaffold Protein Complexes, Claire L. Standen, Norman J. Kennedy, Richard A. Flavell, Roger J. Davis

Open Access Articles

Scaffold proteins have been established as important mediators of signal transduction specificity. The insulin receptor substrate (IRS) proteins represent a critical group of scaffold proteins that are required for signal transduction by the insulin receptor, including the activation of phosphatidylinositol 3 kinase. The c-Jun NH(2)-terminal kinase (JNK)-interacting proteins (JIPs) represent a different group of scaffold molecules that are implicated in the regulation of the JNK. These two signaling pathways are functionally linked because JNK can phosphorylate IRS1 on the negative regulatory site Ser-307. Here we demonstrate the physical association of these signaling pathways using a proteomic approach ...


Mcl-1 Integrates The Opposing Actions Of Signaling Pathways That Mediate Survival And Apoptosis, Caroline Morel, Scott M. Carlson, Forest M. White, Roger J. Davis May 2009

Mcl-1 Integrates The Opposing Actions Of Signaling Pathways That Mediate Survival And Apoptosis, Caroline Morel, Scott M. Carlson, Forest M. White, Roger J. Davis

Open Access Articles

Mcl-1 is a member of the Bcl2-related protein family that is a critical mediator of cell survival. Exposure of cells to stress causes inhibition of Mcl-1 mRNA translation and rapid destruction of Mcl-1 protein by proteasomal degradation mediated by a phosphodegron created by glycogen synthase kinase 3 (GSK3) phosphorylation of Mcl-1. Here we demonstrate that prior phosphorylation of Mcl-1 by the c-Jun N-terminal protein kinase (JNK) is essential for Mcl-1 phosphorylation by GSK3. Stress-induced Mcl-1 degradation therefore requires the coordinated activity of JNK and GSK3. Together, these data establish that Mcl-1 functions as a site of signal integration between the ...


Increasingly Transformed Mcf-10a Cells Have A Progressively Tumor-Like Phenotype In Three-Dimensional Basement Membrane Culture, Karen M. Imbalzano, Iva Tatarkova, Anthony N. Imbalzano, Jeffrey A. Nickerson Mar 2009

Increasingly Transformed Mcf-10a Cells Have A Progressively Tumor-Like Phenotype In Three-Dimensional Basement Membrane Culture, Karen M. Imbalzano, Iva Tatarkova, Anthony N. Imbalzano, Jeffrey A. Nickerson

Open Access Articles

BACKGROUND: MCF-10A cells are near diploid and normal human mammary epithelial cells. In three-dimensional reconstituted basement membrane culture, they undergo a well-defined program of proliferation, differentiation, and growth arrest, forming acinar structures that recapitulate many aspects of mammary architecture in vivo. The pre-malignant MCF-10AT cells and malignant MCF-10CA1a lines were sequentially derived from the MCF-10A parental cell line first by expression of a constitutively active T24 H-Ras generating the MCF-10AT cell line. This was followed by repeated selection for increasingly aggressive tumor formation from cells recovered from xenograft tumors in immuno-compromised mice, generating the MCF-10CA1a cell line. When inoculated subcutaneously ...


Supervillin Reorganizes The Actin Cytoskeleton And Increases Invadopodial Efficiency, Jessica Lynn Crowley, Tara C. Smith, Zhiyou Fang, Norio Takizawa, Elizabeth J. Luna Feb 2009

Supervillin Reorganizes The Actin Cytoskeleton And Increases Invadopodial Efficiency, Jessica Lynn Crowley, Tara C. Smith, Zhiyou Fang, Norio Takizawa, Elizabeth J. Luna

Open Access Articles

Tumor cells use actin-rich protrusions called invadopodia to degrade extracellular matrix (ECM) and invade tissues; related structures, termed podosomes, are sites of dynamic ECM interaction. We show here that supervillin (SV), a peripheral membrane protein that binds F-actin and myosin II, reorganizes the actin cytoskeleton and potentiates invadopodial function. Overexpressed SV induces redistribution of lamellipodial cortactin and lamellipodin/RAPH1/PREL1 away from the cell periphery to internal sites and concomitantly increases the numbers of F-actin punctae. Most punctae are highly dynamic and colocalize with the podosome/invadopodial proteins, cortactin, Tks5, and cdc42. Cortactin binds SV sequences in vitro and contributes ...