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Various Cellular Functions (various + cellular_function)
Selected AbstractsMBSJ MCC Young Scientist Award 2009 REVIEW: Selective autophagy regulates various cellular functionsGENES TO CELLS, Issue 9 2010Masaaki Komatsu Autophagy is a self-eating system conserved among eukaryotes, in which cellular components including organelles are entrapped into a double membrane structure called the autophagosome and then degraded by lysosomal hydrolases. In addition to its role in supplying amino acids in response to nutrient starvation, autophagy is involved in quality control to maintain cell health. Thus, inactivation of autophagy causes the formation of cytoplasmic protein inclusions, which comprise misfolded proteins and the accumulation of many degenerated organelles, resulting in liver injury, diabetes, myopathy and neurodegeneration. Furthermore, although autophagy has been considered nonselective, increasing evidence points to the selectivity of autophagy in sorting vacuolar enzymes and removal of aggregate-prone proteins and unwanted organelles. Such selectivity allows diverse cellular regulation, similar to the ubiquitin proteasome pathway. In this review, we discuss the physiological roles of selective autophagy and their molecular mechanisms. [source] Physical and functional interaction between mortalin and Mps1 kinaseGENES TO CELLS, Issue 6 2007Masayuki Kanai Mortalin is a member of Hsp70 chaperoning protein family involved in various cellular functions. Through the search of the kinases that mortalin physically interact with, we identified Mps1 as such a kinase. Mps1 kinase has been implicated in the regulation of centrosome duplication and mitotic checkpoint response. Mortalin binds to Mps1, and is phosphorylated by Mps1 on Thr62 and Ser65. The phosphorylated mortalin then super-activates Mps1 in a feedback manner. Mortalin has been previously shown to localize to centrosomes, and to be involved in the regulation of centrosome duplication. We found that centrosomal localization of mortalin depends on the presence of Mps1. Moreover, Mps1-associated acceleration of centrosome duplication depends on the presence of mortalin and super-activation by the Thr62/Ser65 phosphorylated mortalin. [source] Generation of cortactin floxed mice and cellular analysis of motility in fibroblastsGENESIS: THE JOURNAL OF GENETICS AND DEVELOPMENT, Issue 9 2009Shinji Tanaka Abstract Cortactin is an F-actin binding protein that has been suggested to play key roles in various cellular functions. Here, we generated mice carrying floxed alleles of the cortactin (Cttn) gene (Cttnflox/flox mice). Expression of Cre recombinase in mouse embryonic fibroblasts (MEFs) isolated from Cttnflox/flox embryos depleted cortactin within days, without disturbing F-actin distribution and localization of multiple actin-binding proteins. Cre-mediated deletion of Cttn also did not affect cell migration. To obtain mice with a Cttn null allele, we next crossed Cttnflox/flox mice with transgenic mice that express Cre recombinase ubiquitously. Western blot and immunocytochemical analysis confirmed complete elimination of cortactin expression in MEFs carrying homozygously Cttn null alleles. However, we found no marked alteration of F-actin organization and cell migration in Cttn null-MEFs. Thus, our results indicate that depletion of cortactin in MEFs does not profoundly influence actin-dependent cell motility. genesis 47:638,646, 2009. © 2009 Wiley-Liss, Inc. [source] p53 may positively regulate hepatocyte proliferation in ratsHEPATOLOGY, Issue 2 2002Yukiko Inoue p53, known as a tumor suppressor gene, is a transcription factor that regulates various cellular functions. Recently, several growth factor gene promoters, including that of transforming growth factor , (TGF-,), were shown to be direct targets of p53-mediated transcription. Hepatic p53 mRNA is up-regulated during liver regeneration in rats. The aim of this study is to examine the role of p53 in hepatocyte proliferation. p53 protein levels were examined in rat hepatocytes cultured in the medium containing hepatocyte growth factor (HGF). p53 levels began to increase after 6 hours of incubation, reached a maximum at 18 hours, and decreased thereafter. DNA synthesis increased at 12 hours and peaked at 30 hours. When hepatocytes were incubated with p53 antisense oligonucleotide in addition to HGF, increases of p53 and TGF-, levels were suppressed, and DNA synthesis was reduced. The increases of TGF-, levels and DNA synthesis were also suppressed by a chemical inhibitor of p53, pifithrin-,. In rats after two-thirds partial hepatectomy, hepatic p53 increased and reached maximal levels around 16 hours when hepatic HGF levels have been shown to reach a maximum followed by an increase in hepatic TGF-, levels or hepatocyte proliferation. In contrast, sham-operated rats showed minor elevations of hepatic p53 levels. In conclusion, p53 production is stimulated by HGF and may contribute to the proliferation of rat hepatocytes. Considering previous findings indicating the importance of endogenous TGF-, for the proliferation of hepatocytes stimulated by HGF, TGF-, might play a role in HGF-p53 mediated hepatocyte proliferation. [source] Proteomics of human umbilical vein endothelial cells applied to etoposide-induced apoptosisPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 15 2005Arnaud Bruneel Dr. Abstract We have undertaken to continue the proteomic study of human umbilical vein endothelial cells (HUVECs) using the combination of 2-DE, automated trypsin digestion, and PMF analysis after MALDI-TOF MS and peptide sequencing using nano LC-ESI-MS/MS. The overall functional characterization of the 162 identified proteins from primary cultures of HUVECs confirms the metabolic capabilities of endothelium and illustrates various cellular functions more related to cell motility and angiogenesis, protein folding, anti-oxidant defenses, signal transduction, proteasome pathway and resistance to apoptosis. In comparison with controls cells, the differential proteomic analysis of HUVECs treated by the pro-apoptotic topoisomerase inhibitor etoposide further revealed the variation of eight proteins, namely, GRP78, GRP94, valosin-containing protein, proteinase inhibitor 9, cofilin, 37-kDa laminin receptor protein, bovine apolipoprotein, and tropomyosin. These data suggest that etoposide-induced apoptosis of human vascular endothelial cells results from the intricate involvement of multiple apoptosis processes including at least the mitochondrial and the ER stress pathways. The presented 2-D pattern and protein database, as well as the data related to apoptosis of HUVECs, are available at http://www.huvec.com. [source] Purification, crystallization and initial X-ray diffraction study of human REV7 in complex with a REV3 fragmentACTA CRYSTALLOGRAPHICA SECTION F (ELECTRONIC), Issue 12 2009Kodai Hara REV7 is involved in various cellular functions including DNA replication, signal transduction and cell-cycle regulation. In DNA replication, REV7 interacts with REV3 and forms DNA polymerase ,, which plays a central role in error-prone DNA synthesis. REV3 is a catalytic subunit and its activity is stimulated by REV7. To clarify the structural basis of the interaction between REV7 and REV3, human REV7 was crystallized in complex with a REV3 fragment. Two crystal forms were obtained. Crystal forms I and II belonged to space groups P21, with unit-cell parameters a = 43.8, b = 50.0, c = 107.3,Å, , = 96.9°, and P41212 or P43212, with unit-cell parameters a = b = 76.6, c = 118.4,Å, respectively. [source] | |||||||||||||