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本帖最后由 lingn 于 2010-6-30 20:13 编辑
. @% f7 X9 V8 L* r中科院裴端卿研究组成功制造非“yamanaka factor”的iPS细胞。虽然已经不是那么令人supprising了,但还是不 ...- c+ C. G2 t: B8 `8 Q% h3 w
sususu 发表于 2010-6-30 16:18  2 |: m' x4 U' o
Ding sheng在PNAS上有一篇文章和这个有点类似,发现human ESC更多的依赖E-cadherin,比较少的依赖integrin。
, ]( ? _ P7 U: P7 W: LProc Natl Acad Sci U S A. 2010 May 4;107(18):8129-34. Epub 2010 Apr 20.
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$ j) X# Y. O# r; T- l- c5 ARevealing a core signaling regulatory mechanism for pluripotent stem cell survival and self-renewal by small molecules.+ k/ C9 F d4 _4 g+ ]- Z- C" e" E' d
Xu Y, Zhu X, Hahm HS, Wei W, Hao E, Hayek A, Ding S.
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Department of Chemistry, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.! m3 A2 e. j" o5 Q' `
% ] ^- L+ c: N! [, b0 F/ wAbstract7 e! J$ C, B+ A. y' A# d J: X
Using a high-throughput chemical screen, we identified two small molecules that enhance the survival of human embryonic stem cells (hESCs). By characterizing their mechanisms of action, we discovered an essential role of E-cadherin signaling for ESC survival. Specifically, we showed that the primary cause of hESC death following enzymatic dissociation comes from an irreparable disruption of E-cadherin signaling, which then leads to a fatal perturbation of integrin signaling. Furthermore, we found that stability of E-cadherin and the resulting survival of ESCs were controlled by specific growth factor signaling. Finally, we generated mESC-like hESCs by culturing them in mESC conditions. And these converted hESCs rely more on E-cadherin signaling and significantly less on integrin signaling. Our data suggest that differential usage of cell adhesion systems by ESCs to maintain self-renewal may explain their profound differences in terms of morphology, growth factor requirement, and sensitivity to enzymatic cell dissociation.
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