Alternative splicing of cyclin D1 gene mRNA has recently been demonstrated. The novel transcript shows no splicing at the downstream exon 4 boundary and encodes a protein with an altered carboxyl-terminal domain that is a cyclin D1 variant; exon 5 is not included in the coding sequence which terminates downstream of exon 4. We here produced cells that exogenously express each form of cyclin D1 and analysed their cell cycle regulation. We found that (1) alternative splicing forms of cyclin D1 modulated entry into the cell cycle in an inverse manner; (2) both splicing forms suppressed cell growth; and (3) cells overexpressing form [a] were inhibited from entry into and completion of the S phase, although form [b]-expressing cells showed no reduction of G1-to S transition. We also found that overexpression of either cyclin D1 form upregulated Rb gene products, suggesting that this upregulation may be one of the causes of growth suppression in cyclin D1 overexpressing cells.
We clarified basic trends of age- and gender-related amino acid concentrations in serum. In normal healthy Japanese people who ate normally and lived an independent life, there are significant age- and gender-related differences.
The mechanism of C−O bond cleavage of allylic alcohols promoted by the hydridopalladium
complexes PdH(OTf)(DPCB-Y) (2), bearing 1,2-diaryl-3,4-bis[(2,4,6-tri-tert-butylphenyl)phosphinidene]cyclobutene ligands (DPCB-Y), has been investigated (aryl = 4-(trifluoromethyl)phenyl (DPCB-CF3), phenyl (DPCB), 4-methoxyphenyl (DPCB-OMe), 4-octyloxyphenyl
(DPCB-OOct)). This reaction forms the (π-allyl)palladium complexes [Pd(π-allyl)(DPCB-Y)]OTf (1), which are key intermediates for the catalytic allylation of aniline with allylic alcohols.
The platinum analogue of 2 is obtained as the hydrido-bridged dimer [Pt2(μ-H)2(DPCB)2](OTf)2 (4) by the treatment of PtMe(OTf)(DPCB) (5) with HSiMe2Ph in the presence of a
small amount of water. Complex 4 cleaves the C−O bond of allylic alcohols at 50 °C, yielding
the π-allyl complexes [Pt(π-allyl)(DPCB)]OTf (7). Although complex 2, similarly prepared
by the reaction of PdMe(OTf)(DPCB) (5) with HSiMe2Ph and water, is too unstable to be
identified, its formation is confirmed by trapping experiments using dienes to give the
corresponding π-allyl complexes. Complex 2, thus generated, instantly reacts with allylic
alcohols at room temperature to afford the π-allyl complex 1 in high yield. The intermediacy
of 2 in the catalytic allylation is further examined by kinetic experiments on actual catalytic
systems, leading to mechanistic details of C−O bond cleavage promoted by 2.
The effects of sodium butyrate (SB) and trichostatin A (TSA) on cell proliferation andapoptosis against human glioma T98G, U251MG, and U877MG cells were investigated. Upon exposure to either SB or TSA, cell proliferation was reduced, and apoptosis detected by DNA fragmentation analysis and the cleavage of CPP32 was induced. Previously, we reported that SB increased the expression levels of p21 (WAF-1) and inhibited G1-S transition of the cell cycle. In this study, we showed that TSA also increased p21 expression, suggesting that histone deacetylase (HDAC) inhibitors may up-regulate p21 protein in common and thus arrest proliferation in the G1 phase of the cell cycle. To further determine the underlying molecular mechanisms of apoptosis with either SB or TSA treatment, we studied the expression levels of apoptosis-related proteins in human glioma cells. SB increased the expression of the Bad protein, although the expression of Bcl-2, Bcl-xL, Bax, and Fas was not changed by theaddition of SB. TSA treatment also up-regulated the expression of Bad protein. The results suggest that HDAC inhibitors such as SB and TSA induce apoptosis through an increase in Bad protein in human glioma cells in vitro.
The genome of Red clover necrotic mosaic virus (RCNMV) consists of RNA1 and RNA2, both lacking a cap structure and a poly(A)tail. RNA1 has a translational enhancer element (3'TE-DR1) in the 3' untranslated region (UTR). In this study, we analyzed the roles of 5' and 3' UTRs of RNA1 in 3'TE-DR1-mediated cap-independent translation in cowpea and tobacco BY-2 protoplasts using a dual-luciferase (Luc) reporter assay system. Most mutations introduced into RNA1 5' UTR in reporter Luc mRNA abolished or greatly reduced cap-independent translation in BY-2 protoplasts, whereas those mutations had no or much milder effects if any on translational activity in cowpea protoplasts. Our results suggest that a stem-loop structure predicted in the 5' proximal region of RNA1 plays important roles in both translation and RNA stability. We also show that 3'TE-DR1-mediated cap-independent translation relies on a ribosome-scanning mechanism in both protoplasts.
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