阎润涛果然是说到做到,不停地指控小颜剽窃了自己的成果,本人已在前面大阎你越红线了>一文中指出反复错误地用文字形式指控她人剽窃是诽谤(It is LIBEL to FALSELY accuse someone of plagrarism IN WRITING!),劝他悬崖勒马,等《自然》杂志回信再来给大家一个说明。可他不但不停,反而变本加厉,发动新一轮的抹黑。
首先,大阎一直在纠结小颜在讲课时用得那照片上的那个开口朝上和朝下的图,指出那是他提出的喇叭口模型,其实不过是一个弥天大谎,这个模型是很早就被人提出的“alternate access”模型,其中一个比较有名的是Rocker switch model (见图)。大阎在《细胞》上“第一次”提出的模型既不是第一次,也不是新模型,而是在做了一系列的氨基酸突变试验发现一个半胱氨酸(C256)比较重要之后对模型进行了修正,仅此而已。即使有人说他们做的好,也是反映当时的水平,做的突变比较全面,这个我们在城里和大阎意见相左的人也没有否认,但是,承认这点并不是说大阎提出一个修正模型后别人就不能再修正了,此其一。
While there is no doubt the two papers published by Yan & Maloney contributed significantly to the advancement in our understanding of secondary transport mechanism in general at the time (as noted by Mueckler1999), the importance and the relevance of their contribution seems to have faded over time, as it wasn’t cited by numerous paper by Mueckler 2009 and the references therein. Yan & Maloney was also not cited by two seminal reviews. Forrest et al. and Law et al. Maloney was one of the authors in the latter.
A cursory survey of past literature, some of which cited by this paper, also reveals numerous papers with similar schematic depiction of the Alternating Access by MFS proteins (Dang, Forrest, Iancu, Madej, Nie). In particular, Dang et al. came from Dr. Nieng Yan’s lab was published in 2010, prior to the critical year of 2012 mentioned in Runtao Yan’s comments, and contradict his claim.
Fanreninus 发表评论于
回复 'SwiperTheFox' 的评论 : I saw your "test" comment there. It is very quiet, just one guy saying: "A YRT's fan from WXC, I hereby give my unconditional, continuing support to YRT. This is also to prove that here is an open platform where everyone can post comments at whatever time and in whatever way one pleases."
回复 'JessAB' 的评论 : Thanks! I won't go there. I don't think that people will take him seriously when they look at how unprofessional his letter or comment is.
JessAB 发表评论于
After reading R. Yan’s most recent comments in his own blog, I change my mind. Now I think anyone who has expertise in this field with good English writing and also disagrees with R Yan’s comments posted in Nature website can go there to give rebuttals of the points he had made.
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In 2012, Dr Maloney (Hopkins team) was alive. The Tsinghua team had to cite our papers if they provided the working model, which should be the same as ours. In such consideration, they may worry that the paper could not be accepted by Nature as it just confirmed our model. Dr Maloney died Dec.12, 2013, and Tsinghua team’s 2014 Nature paper was published on May 18, 2014, which showed the glucose transporter working model.
回复 'JessAB' 的评论 : Thanks for letting me know! The letter was surprisingly WEAK. I wouldn't bother to respond to it at Nature.com. But I did write a new blog a couple of minutes ago in response to it for public consumption. It is only intended for readers in WXC! :)
I just read R. Yan’s comment in the Nature paper link. I think we should not rebut him in the link because it may not be appropriate (just my 2 cents).
老阎自己要先冷静。小颜成果是结晶,机理是附加值。小颜说了,机理证据需进一步获取。如果别人像老阎那样用他的逻辑逐字逐句攻他的老文章,他就没法招架了。首先喇叭口不是他的,他老板更推荐gated pore, 他的探针不是实际的底物,因此他的结果也是假设之上,待证。他老板从八十年代到至少2002还在研究同一个转运体,也就是说老阎93-95年并没有解决这一个转运体的大部分问题就离开了老板。更有意义的是,在更新的研究中他老板不提老阎的93-95的发现,a residual C265, 也不引他93-96文章,见下2002文。也许这就老阎说的雪藏。不知道为什么。但老阎应该自己知道,那就该停下了。留下好的回忆吧。更不要怪小颜。Microbial Cell Biology
Pyridoxal 5-Phosphate Inhibition of Substrate Selectivity Mutants of UhpT, the Sugar 6-Phosphate Carrier of Escherichia coli
Jason A. Hall, Peter C. Maloney
DOI: 10.1128/JB.184.13.3756-3758.2002
Because there is as yet no crystallographic structure to guide an analysis, the study of helix relationships and helix function in members of the MFS has relied heavily on site-directed mutagenesis and the modification chemistry it affords.
We have applied these techniques to the study of UhpT, the Pi-linked hexose phosphate antiport carrier of Escherichia coli (14, 15, 21). In previous work, Asp388 and Lys391, located in the 11th transmembrane segment (TM11) of this transporter, were identified as participants in an intrahelical salt bridge (7). Study of this ion pair indicated that both positions 388 and 391 might lie on the UhpT translocation pathway since D388C and K391C single-cysteine variants are sensitive to the membrane impermeant, thiol-reactive probe p-chloromercuribenzosulfonate but are unaffected when treatment is in the presence of substrate (8). Further analysis indicated that these two positions might also function as determinants of substrate specificity.