科技部: 都说了是“图片误用”，tmd，烦死了！
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FROM 64.120.119.*

饶教授一直是我尊敬的人，听过他的多次演讲。
【 在 wanwan82 的大作中提到: 】
: https://mp.weixin.qq.com/s/tfK1GQL3y9XRUEol9z6ShA
:  
: 【 在 zgpat (书剑飘零) 的大作中提到: 】
: ....................

- 来自「最水木 for iPhone 6」
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FROM 223.104.20.*

向饶致以敬意，无论如何，能够勇敢站起来的人不多


【 在 wanwan82 的大作中提到: 】
: 嗯！真是有血性的汉子！
: 仰慕
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FROM 120.245.116.*

按你这逻辑，造假的都可以说试验做错了？或者图片误用了？那就没有造假了？

【 在 zhenniub 的大作中提到: 】
: 但是这个好像不易证明这是造假啊。裴钢说试验做错了也可以把
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FROM 223.72.70.76

虽然我基本不懂，但也能从abstract看出根本就不是一次假阳性这种，而就是造假


ABSTRACT The putative seven-transmembrane (TM) domains have been the structural hallmark for the superfam- ily of heterotrimeric G protein-coupled receptors (GPCRs) that regulate a variety of cellular functions by mediating a large number of extracellular signals. Five-TM GPCR mu- tants of chemokine receptor CCR5 and CXCR4, the N- terminal segment of which connected directly to TM3 as a result of a deletion of TM1–2 and the first intracellular and extracellular loops, have been obtained in this study. Laser confocal microscopy and flow cytometry analysis revealed that these five-TM mutant GPCRs were expressed stably on the cell surface after transfection into human embryonic kidney 293 cells. The five-TM CCR5 and CXCR4 functioned as normal chemokine receptors in mediating chemokine- stimulated chemotaxis, Ca2+ influx, and activation of pertus- sis toxin-sensitive G proteins. Like the wild-type GPCRs, the five-TM mutant receptors also underwent agonist-dependent internalization and desensitization and were subjected to regulation by GPCR kinases and arrestins. Our study indi- cates that five-TM domains, at least in the case of CCR5 and CXCR4, appear to meet the minimum structural requirements for a functional GPCR and suggests possible existence of functional five-TM GPCRs in nature during evolution.

【 在 spritesw 的大作中提到: 】
: 也可能是一次假阳性没重复就发表了，属于失误，不属于造假
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FROM 123.113.31.*