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Domains Rich (domain + rich)
Selected AbstractsCombination of Clk family kinase and SRp75 modulates alternative splicing of Adenovirus E1AGENES TO CELLS, Issue 3 2008Jun-ichiro Yomoda SR proteins are non-snRNP splicing factors harbouring a domain rich in Arg-Ser repeats, which are extensively phosphorylated by several kinases. We performed a comparative study of different SR kinases, including SRPK, Clk, PRP4 and DYRK, and found that only Clks efficiently altered 5, splice site selection of Adenovirus E1A. The phosphorylation state of SR proteins was examined using a phospho-SR specific antibody mAb1H4 and a 75 kDa protein was most evidently hyperphosphorylated by Clks. Administration of TG003, a specific inhibitor for the Clk family members, specifically and rapidly induced dephosphorylation of 75 kDa SR protein. Imaging with mRFP-SRp75 in living cells revealed that its nuclear distribution was rapidly altered upon inhibition of the Clk activity by TG003. Co-transfection experiments demonstrated that HA-tagged SRp75 was hyperphosphorylated by Clk family members, but not by other SR kinases. These results indicate that Clks specifically hyperphosphorylate SRp75. Furthermore, SRp75 over-expression promoted the selection of 12S 5, splice site in E1A pre-mRNA, which is stimulated by co-expression of Clks. These results suggest that the specific combination of SR protein and SR kinase plays a distinct role in alternative splicing through dynamic balance of phosphorylation. [source] Vesicles as reactors of nanoparticles: an anomalous small-angle X-ray scattering study of the domains rich in copper ionsJOURNAL OF APPLIED CRYSTALLOGRAPHY, Issue 2007Attila Bóta The formation of copper hydroxide and copper oxide particles in the gaps among the stacks of multilamellar vesicles is described, illustrating a new pathway in the preparation of nanometre-scale particles. The in situ structural characterization of both the solid particles and the vesicles as a reaction medium was performed in the initial and final states of the process by using anomalous small-angle X-ray scattering (ASAXS) and freeze-fracture methods. The ASAXS method provides a description of the particle-size distribution of the copper nanoparticles, in spite of the fact that they are present in low concentration. This method allows the particle formation and growth to be monitored throughout the whole time range of the synthesis. [source] Low-temperature bitumen stiffness and viscous paraffinic nano- and micro-domains by cryogenic AFM and PDMJOURNAL OF MICROSCOPY, Issue 3 2007J-F. MASSON Summary In an effort to better understand the structure and behaviour of bitumen in low temperature, we describe the first use of cryogenic atomic force microscopy and phase detection microscopy to characterize bitumen nano- and micro-structures. The results were interpreted in light of glass transition temperatures (Tgs) for bitumen fractions. The domains visible by microscopy, the catana, peri and para phases, were attributed to domains rich in asphaltenes, naphthene and polar aromatics, and saturates, respectively. Between ,10°C and ,30°C, atomic force microscopy images revealed topographic features not visible in atomic force microscopy images acquired at room temperature. According to phase detection microscopy and Tgs, the features were assigned to viscous unfrozen saturates. Upon cooling to ,72°C, unfrozen domains of 20,400 nm were observed. These domains were found in the paraphase rich in saturates and in the periphase rich in naphthene aromatics and polar aromatics. The findings indicate that new viscous domains form upon cooling to low temperatures owing to phase segregation, and that some bitumens are never entirely rigid in low temperatures. [source] cAMP-induced differentiation of human neuronal progenitor cells is mediated by nuclear fibroblast growth factor receptor-1 (FGFR1)JOURNAL OF NEUROCHEMISTRY, Issue 6 2003E. K. Stachowiak Abstract Activation of cAMP signaling pathway and its transcriptional factor cyclic AMP response element binding protein (CREB) and coactivator are key determinants of neuronal differentiation and plasticity. We show that nuclear fibroblast growth factor receptor-1 (FGFR1) mediates cAMP-induced neuronal differentiation and regulates CREB and CREB binding protein (CBP) function in ,-internexin-expressing human neuronal progenitor cells (HNPC). In proliferating HNPC, FGFR1 was associated with the cytoplasm and plasma membrane. Treatment with dB-cAMP induced nuclear accumulation of FGFR1 and caused neuronal differentiation, accompanied by outgrowth of neurites expressing MAP2 and neuron-specific neurofilament-L protein and enolase. HNPC transfected with nuclear/cytoplasmic FGFR1 or non-membrane FGFR1(SP-/NLS), engineered to accumulate exclusively in the cell nucleus, underwent neuronal differentiation in the absence of cAMP stimulation. In contrast, FGFR1/R4, with highly hydrophobic transmembrane domain of FGFR4, was membrane associated, did not enter the nucleus and failed to induce neuronal differentiation. Transfection of tyrosine kinase-deleted dominant negative receptor mutants, cytoplasmic/nuclear FGFR1(TK-) or nuclear FGFR1(SP-/NLS)(TK-), prevented cAMP-induced neurite outgrowth. Nuclear FGFR1 localized in speckle-like domains rich in phosphorylated histone 3 and splicing factors, regions known for active RNA transcription and processing, and activated the neurofilament-L gene promoter. FGFR1(SP-/NLS) transactivated CRE, up-regulated phosphorylation and transcriptional activity of CREB and stimulated the activity of CBP several-fold. Thus, cAMP-induced nuclear accumulation of FGFR1 provides a signal that triggers molecular events leading to neuronal differentiation. [source] A major breakpoint cluster domain in murine radiation-induced acute myeloid leukemia,MOLECULAR CARCINOGENESIS, Issue 2 2002Rosemary Finnon Abstract Cytogenetic and molecular studies have provided evidence of the clustering of chromosome 2 deletion breakpoints in radiation-induced murine acute myeloid leukemia (AML). Moreover, clustering occurs in at least two fragile domains rich in telomere-like arrays. Here we describe a physical map of the distal breakpoint cluster and confirm the presence of inverted head-to-head telomeric sequence arrays. These potentially recombinogenic sequences were not, however, the direct focus for post-irradiation chromosome breakage in AML. Instead, the two arrays bordered a 2.5-kb sequence with properties expected of a nuclear matrix attachment region (MAR). The putative MAR co-localized in the fragile domain with genes important to the hemopoietic system (leukocyte tyrosine kinase, zinc finger protein 106, erythrocyte protein band 4.2, and ,2 -microglobulin (,2m)); the ,2m subdomain was a particular focus of breakage. On the basis of these and other data, we suggest that AML-associated chromosome 2 fragility in the mouse is a consequence of domain-specific fragility in genomic domains containing numerous genes critical to the hemopoietic system. Copyright © Crown Copyright 2002. Recorded with the permission of the controller of Her Majesty's Stationery Office. Published by Wiley-Liss, Inc. [source] | |||||||||||||