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[资源] 《细胞》【Cell】2013年04月25日全文PDF版本

《细胞》【Cell】2013年04月25日全文PDF版本
Brain Origami Master
PAGE 535
During evolution, the mammalian brain has undergone enormous expansion, with correspondingchanges in gyrification (folding). Stahl et al. show that levels of a DNA-associatedprotein, Trnp1, determine whether the cortex expands tangentially or radially and alsoregulate its gyrification. Trnp1 levels in the developing human brain correlate with regionallevels of folding.
TNF Excess: TB or Not TB
PAGE 521
Tumor necrosis factor has been shown to be protective in tuberculosis. Roca and
Ramakrishnan find that excess TNF levels, however, induce mitochondrial ROS and leadto macrophage necroptosis. This results in the lysis of infected macrophages and releaseof mycobacteria into the extracellular milieu, where they are able to grow unfettered. Pharmacological modulation of necroptosismay help to preserve macrophage microbicidal activity and confer tuberculosis resistance to individuals with excess TNF.
Cell Sorting Nixes Noise in Development
PAGE 550
Patterning and morphogenesis often occur concurrently in development. Using in toto imaging in the zebrafish neural tube, Xionget al. show that cell movements during morphogenesis create ‘‘noise’’ in the positional information encoded by the Sonic hedgehogmorphogen gradient. As a result, cells of different fates are specified in mixed and overlapping patterns. Fate-specific cell movementshen create sharp boundaries between cell-type domains. Thus, morphogenetic cell movements can both limit and correctpositional information.
RNA Editor Meets RNA Silencer
PAGE 575
ADAR1 is a homodimeric RNA-editing enzyme that converts adenosine to inosine in dsRNA. Ota et al. now show that ADAR1 alsoplays a completely different role as an RNAi regulator. When an ADAR1 monomer forms a complex with Dicer, it acts as an RNAsilencer by promoting miRNA processing, RISC loading, and RNAi efficacy. miRNA expression is globally suppressed in mouseembryos lacking ADAR1, altering expression of miRNA targets and contributing to embryonic lethality.Vitamins Smack Down SMAD in Liver Injury
PAGE 601
Ding et al. show that vitamin D receptor (VDR) signaling inhibits liver fibrosis (scarring) by antagonizing the action of SMAD transcriptional
regulators in hepatic stellate cells. SMADs are activated by liver injury and, in the absence of VDR ligands, activate profibroticgenes. However, they also enable their own repression by making the chromatin around their target sites more accessible to VDR thatwill bind and inhibit SMAD activity in the presence of VDR ligands.
Tanking the Proteasome
PAGE 614
Selective protein degradation by the ubiquitin-proteasome system plays a vital role in
cellular homeostasis. Defects in this process are associated with various human diseases,and the proteasome is a validated drug target in cancer therapy. Cho-Park and Stellershow that Tankyrase-mediated ADP-ribosylation of PI31 activates proteasomes bypromoting 26S proteasome assembly and that this process can be blocked withTankyrase-inhibitors. These results reveal a mechanism of proteasome regulation thatcan be targeted with existing small-molecule inhibitors.[ 来自科研家族生物医药家族 ]

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附件 1 : Cell2013-4-25.pdf

2013-04-27 09:38:51, 34.46 M

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