Reply: To PMID 24849310.
Reply: To PMID 24849310.
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回复：PMID 24849310。
DOI：
10.1002/hep.27430
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Diehl,AnnaMae
中科院分区：
文献类型：
--
作者：
Guy,Cynthia;Suzuki,Ayako;Abdelmalek,Manal;Burchette,James;Diehl,AnnaMae
Guy等人的文章1很好地说明了非酒精性脂肪性肝炎（NASH）患者结局的改善与Sonic Hedgehog（SHH+）细胞数量的减少相关。此外，GLI 2 + SOX 9+肝祖细胞的数量也趋于减少。1我们对这些数据感到兴奋，这些数据表明，SHH配体暴露的减少降低了小管反应的强度。然而，我们希望解决仅使用GLI 2作为Hedgehog（Hh）响应细胞的标志物的局限性。经典Hh途径信号在Hh配体与其受体Patched 1（PTCH 1）结合后转导，导致Smoothened（SMO）的去抑制和激活。结果是GLI蛋白（GLI 1、GLI 2、GLI 3）稳定为转录激活因子，并使Hh靶基因表达。在脊椎动物中，Hh配体信号转导成GLI介导的转录反应发生在SMO易位到初级纤毛（Pc）中之后。2这是值得考虑的，因为GLI介导的转录反应可以独立于Hh/PTCH 1/Pc/SMO级联驱动。3
The article by Guy et al. 1 nicely illustrated improved nonalcoholic steatohepatitis (NASH) patient outcomes correlated with a decrease in Sonic Hedgehog (SHH+) cell numbers. Further, the number of GLI2+ SOX9+ liver progenitor cells also tended to decrease. 1 We are excited by these data, which suggest that an association between a decrease in exposure to SHH ligand reduces the intensity of the ductular reaction. However, we would like to address the limitations of using only GLI2 as a marker of Hedgehog (Hh)-responsive cells.The canonical Hh pathway signal is transduced following Hh ligand binding to its receptor, Patched1 (PTCH1), leading to the derepression and activation of Smoothened (SMO). The result is stabilization of GLI proteins (GLI1, GLI2, GLI3) into transcriptional activators, and Hh target gene expression. In vertebrates, transduction of Hh ligand signal into a GLI-mediated transcriptional response occurs following SMO translocation into the primary cilium (Pc). 2 This is pertinent to consider, as GLI-mediated transcriptional responses can be driven independently of the Hh/PTCH1/Pc/SMO-cascade. 3
DOI：
10.1152/ajpgi.00456.2005
发表时间：
2006-05-01
影响因子：
4.5
作者：
Sicklick, JK;Li, YX;Diehl, AM
通讯作者：
Diehl, AM
DOI：
10.1152/ajpgi.00292.2009
发表时间：
2009-12-01
影响因子：
4.5
作者：
Choi, Steve S.;Omenetti, Alessia;Diehl, Anna Mae
通讯作者：
Diehl, Anna Mae
影响因子：
25.7
作者：
Yang, Liu;Wang, Ying;Diehl, Anna Mae
通讯作者：
Diehl, Anna Mae