CDC25A (Cell division cycle 25A)

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CDC25AQ110del: A Novel Cell Division Cycle 25A Isoform Aberrantly Expressed in Non-Small Cell Lung Cancer

OBJECTIVE Lung cancer remains number one cause of cancer related deaths worldwide. Cell cycle deregulation plays a major role in the pathogenesis of Non-Small Cell Lung Cancer (NSCLC). CDC25A represents a critical cell cycle regulator that enhances cell cycle progression. In this study we aimed to investigate the role of a novel CDC25A transcriptional variant, CDC25A(Q110del), on the regulation...

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Disruption of the checkpoint kinase 1/cell division cycle 25A pathway abrogates ionizing radiation-induced S and G2 checkpoints.

Checkpoint kinase (Chk)1 is an evolutionarily conserved protein kinase that was first identified in fission yeast as an essential component of the DNA damage checkpoint. In mice, Chk1 provides an essential function in the absence of environmentally imposed genotoxic stress. Here we show that human cells lacking Chk1 exhibit defects in both the ionizing radiation (IR)-induced S and G(2) checkpoi...

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Novel Interactions between FOXM1 and CDC25A Regulate the Cell Cycle

FOXM1 is a critical regulator of the G1/S and G2/M cell cycle transitions, as well as of the mitotic spindle assembly. Previous studies have suggested that FOXM1 regulates CDC25A gene transcription, but the mechanism remains unknown. Here, we provide evidence that FOXM1 directly regulates CDC25A gene transcription via direct promoter binding and indirect activation of E2F-dependent pathways. Pr...

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Cell cycle, cell division, and cell death

Hilary A. Collera,b,* and Arshad Desaic,d aDepartment of Molecular, Cell and Developmental Biology, University of California, Los Angeles, Los Angeles, CA 90095; bDepartment of Biological Chemistry, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095; cDepartment of Cellular and Molecular Medicine, University of California, San Diego, La Jolla, CA 92093; dLudwig Cancer Research Cente...

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Hsp90 stabilizes Cdc25A and counteracts heat shock-mediated Cdc25A degradation and cell-cycle attenuation in pancreatic carcinoma cells.

Pancreas cancer cells escape most treatment options. Heat shock protein (Hsp)90 is frequently over-expressed in pancreas carcinomas and protects a number of cell-cycle regulators such as the proto-oncogene Cdc25A. We show that inhibition of Hsp90 with geldanamycin (GD) destabilizes Cdc25A independent of Chk1/2, whereas the standard drug for pancreas carcinoma treatment, gemcitabine (GEM), cause...

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ژورنال

عنوان ژورنال: Atlas of Genetics and Cytogenetics in Oncology and Haematology

سال: 2017

ISSN: 1768-3262

DOI: 10.4267/2042/62938