求science paper一篇，附链接

viv2005

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http://stke.sciencemag.org/cgi/content/abstract/sigtrans;2007/370/pe2

bridgeyangfan

建议你通过电子邮件向通讯作者所要，他们的邮箱：scott.heximer@utoronto.ca and kblumer@cellbiology.wustl.edu

bridgeyangfan

Ischemia induces regulator of G protein signaling 2 (RGS2) protein
/ O( h& d6 p0 s' Y( @4 r& Q; w. cupregulation and enhances apoptosis in astrocytes
$ y! [3 q* ^2 X! Y3 d+ KMehari Endale,1* Sung Dae Kim,1* Whi Min Lee,1 Sangseop Kim,2 Kyoungho Suk,2 Jae Youl Cho,3! S  _- W. G0 |& k& b0 P* s
Hwa Jin Park,4 Yadav Wagley,5 Suk Kim,6 Jae-Wook Oh,5 and Man Hee Rhee1! P, }: R: Z0 p- A( y6 o; d4 S

( T3 z: `6 s" U1 P3 L& t. }  B$ W9 _Endale M, Kim SD, Lee WM, Kim S, Suk K, Cho JY, Park HJ,
6 e! J9 E- p! p0 J" @8 s* h# A: HWagley Y, Kim S, Oh JW, Rhee MH. Ischemia induces regulator of G7 u" _2 a+ C! E# q+ K
protein signaling 2 (RGS2) protein upregulation and enhances apoptosis( c% i* g2 F$ I
in astrocytes. Am J Physiol Cell Physiol 298: C611–C623, 2010. First
9 ^; i, r" q# O& m" Opublished December 23, 2009; doi:10.1152/ajpcell.00517.2008.—Regulator$ K% Z% N1 u( y  `
of G protein signaling (RGS) family members, such as RGS2,
' [: k& I4 k5 f- Zinteract with G
subunits of heterotrimeric G proteins, accelerating& y4 H* }& Z. |
the rate of GTP hydrolysis and attenuating the intracellular signaling: d% L: S6 M( h' @. [
triggered by the G protein-coupled receptor-ligand interaction.+ _- k( M0 ~9 p& N! c2 c4 p
They are also reported to regulate G protein-effector interactions
8 m  l+ W+ |) Band form multiprotein signaling complexes. Ischemic stress-induced, x0 ?; a2 X; B& K; z: K
changes in RGS2 expression have been described in astrocytes,
( m) U9 U! M, |% [0 I, K% d3 O8 }and these changes are associated with intracellular signaling* @3 [& H; i/ g3 H; b
cascades, suggesting that RGS2 upregulation may be an important
) ]. F0 a, T5 Nmechanism by which astrocytes may regulate RGS2 function in! [" x3 q- [& l6 A: j& |
response to physiological stress. However, information on the' M: F$ u  O  q3 g
functional roles of stress-induced modulation of RGS2 protein2 ^5 r7 S- r" i" X2 [
expression in astrocyte function is limited. We report the role of
0 o5 G" X  ?/ {# b* y/ k; cischemic stress in RGS2 protein expression in rat C6 astrocytoma2 }2 U+ @, O) Q1 O, S; j
cells and primary mouse astrocytes. A marked increase in RGS2
; p! q* P$ j, z! t( k  g$ goccurred after ischemic stress induced by chemicals (sodium azide
: I" i$ y" j' _: {" yand 2-deoxyglucose) or oxygen-glucose deprivation (OGD, real
; c' F  v/ M' e+ _ischemia). RGS2 mRNA expression was markedly enhanced by 1
) ~5 n, Q* C2 |$ eh of exposure to chemical ischemia or 6 h of OGD followed by 2
# A4 u% g& b; Q& Ior 6 h of recovery, respectively. This enhanced expression in
1 }, T" I( w7 T' dprimary astrocytes and C6 cells was restored to baseline levels* o- M  N9 j6 f2 n4 p2 ?
after 12 h of recovery from chemically induced ischemic stress or9 ~/ \" h' r' i( B; \
4 – 6 h of recovery from OGD. RGS2 protein was also significantly
+ d0 y% F) @/ O4 D! o$ xexpressed at 12–24 h of recovery from ischemic insult. Ischemiainduced
5 s. P3 S* j5 ^& z% {4 sRGS2 upregulation was associated with enhanced apoptosis.% E, a6 @  ~3 u$ c2 c8 b6 I8 E
It significantly increased annexin V-positive cells, cleaved
# k6 O0 D% R  f# e. N. \' Ncaspase-3, and enhanced DNA ladder formation and cell cycle' t1 t8 u, v) C7 u3 c9 f
arrest. However, a small interfering RNA (siRNA)-mediated RGS2# f+ `; _  a, O  s3 o& H
knockdown reversed the apoptotic cell death associated with ischemia-% |. T2 F2 [8 b/ |  Q
induced RGS2 upregulation. Upregulated RGS2 was significantly7 |. `/ b$ y0 K! ^
inhibited by SB-203580, a p38 MAPK inhibitor. Rottlerin,0 R! e1 i0 {/ o9 A
a potent inhibitor of PKC, completely abrogated the increased0 F. h; d# I/ v
RGS2 expression. We also examine whether ischemia-induced# ~3 d" n! b& \* c9 Q! G; n# r/ w' T) U
RGS2-mediated apoptosis is affected by siRNA-targeted endogenous
2 M, ]: S8 J- {4 j# D6 J" ]% g+ RPKC downregulation or its phosphorylation. Although6 u' q7 f' @. M7 A+ h
RGS2 upregulation was not affected, siRNA transfection significantly
+ O% U2 u0 Y) {; T, y! p1 Q0 @suppressed endogenous PKC mRNA and protein expresexpressions.
* t; s  S: D4 Q9 f$ |Ischemia-induced PKC phosphorylation and caspase-3' A: f! t' c9 b5 m: F5 L  [
cleavage were dose dependently inhibited by PKC knockdown,
3 Z$ Y! t# e  V4 ?9 \and this endogenous PKC suppression reversed ischemia-induced
8 @& t  ^% ~+ ~$ j- Z! {/ zannexin V-positive cells. This study suggests that ischemic stress
* {2 m& \, w- ]" J: W9 j& V& G( Bincreases RGS2 expression and that this condition contributes to: t1 e& k; p4 t8 [, @) b
enhanced apoptosis in C6 cells and primary astrocytes. The signaling- K! n7 ~' b6 H5 s" L' \4 q
it follows may involve PKC and p38 MAPK pathways.) w! v) z- B: F2 k( _
希望对你有用

viv2005

bridgeyangfan 发表于 2011-8-24 07:56
- N9 ]# |5 e' }建议你通过电子邮件向通讯作者所要，他们的邮箱： and

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为什么这样说，难道这个文献没有全文么

quanri1126

回复 viv2005 的帖子! R* A) h: ]: n, `& A

: _9 m: t) @. X9 b找到了

viv2005

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: P& k$ a/ B6 ^, w" |1 p" n) j非常非常感谢，正急需