发信人: bongbongcat (QTpie球踢派), 信区: Biology
标 题: MCBC journal club paper (the 3rd?)
发信站: The unknown SPACE (Tue Feb 4 19:41:16 2003) WWW-POST

BBS一直不通，所以我都快一个礼拜没上来了。今天一看，斑竹已经发信给我要求present
a paper，而且deadline就是今天。虽然晚上了，但我还是met the deadline了吧？
我picked的paper如下：(没有access的请给我来信。）

Nf1 has an essential role in endothelial cells.
Gitler AD, Zhu Y, Ismat FA, Lu MM, Yamauchi Y, Parada LF, Epstein JA.
Nat Genet 2003 Jan;33(1):75-9

very nice genetics experiments. it came out as a big surprise that NF1 played
an essential role in endothelium cells themselves, as it had been thought
previously that it was the neural crest that resulted in the heart defects.

先写这几句，为的是先把paper给present出去。下面的再慢慢说。
bongbongcat


--
※ 来源:．The unknown SPACE bbs.mit.edu．[FROM: 68.81.]
发信人: ghostneuron (synapseIX), 信区: Biology
标 题: Re: MCBC journal club paper (the 3rd?)
发信站: The unknown SPACE (Thu Feb 6 18:19:15 2003) WWW-POST

1. It's a promising method for pathological study of diseases or development
with multi-tissue-specific gene knockout/in technique.
2. In Fig.2L, it showed thinned myocardium in nf1(nc),but not in the
tissue-specific inactivation of nf1 in myocadial cell(not shown), which
suggests nf1 is necessary for myocardium development, but not after some time
point. How about at earlier period of development than this point? So, i
think it's not cautious to conclude that nf1 function in the neural crest is
not required for normal development of the heart.(the last sentence of the
paper).
3. It seems that nf1 functions opposite way on endothelial and myocardial
cells, and why didn't they study cell cycle signals? As a tumor suppressor
gene, it should be a important factor for proliferation or differentiation of
neural crest cells. And the different fates of endothelial and myocardial
cells might origin from different receptor or signal transduction pathways.
4. Why did they choose E10.5-E13.5?


【 在 bongbongcat (QTpie球踢派) 的大作中提到: 】
:
BBS一直不通，所以我都快一个礼拜没上来了。今天一看，斑竹已经发信给我要求present
: a paper，而且deadline就是今天。虽然晚上了，但我还是met the deadline了吧？
: 我picked的paper如下：(没有access的请给我来信。）
:
: Nf1 has an essential role in endothelial cells.
: Gitler AD, Zhu Y, Ismat FA, Lu MM, Yamauchi Y, Parada LF, Epstein JA.
: Nat Genet 2003 Jan;33(1):75-9
:
: very nice genetics experiments. it came out as a big surprise that NF1
played
: an essential role in endothelium cells themselves, as it had been thought
: previously that it was the neural crest that resulted in the heart defects.
:
: 先写这几句，为的是先把paper给present出去。下面的再慢慢说。
: bongbongcat
:
:

--

草不谢荣于春风，木不怨落于秋天。谁挥鞭驱策四运，万物兴歇皆自然。
※ 来源:．The unknown SPACE bbs.mit.edu．[FROM: 195.143.]
发信人: Marble (小石头哥哥), 信区: Biology
标 题: paper help/ call for MCBJC discussion
发信站: The unknown SPACE (Sun Feb 9 20:36:40 2003), 站内信件

folks, a lot of us may be busy. but if you are free and would
like to throw your quarters (usually coins, but the more, the
better), highly appreciate, since that will keep the MCBJC
going. and i think one good thing about MCBJC is that we can
definitely read some good articles and see how people in other
fields than yours work to address questions, and the ideas
might contribute to your project as well.
this Nat Genet paper was short, however, very informative. i
have not read it in detail, and what i can tell is that they
tried to address the cell-auntonomous function of Nf1 and
established the correlation of its function with the phenotypes
observed in the neurofibromatosis type 1 (NF1). Global knockout
of Nf1 results in mid-embryonic lethality and the cardiac
defects were previously attributed to be secondary to cardiac
neural-crest defects. in this work,two tissue-specific Cre
strains were used to address the questions; endothelial-specific
knockout mutations of Nf1 were generated and the phenotype of
cardiovascular abnormalities were recapitulated. meanwhile,
inactivation of Nf1 in the neural crest resulted in tumors
of neural-crest origin similar to that observed in NF1 human
patients. tissue-specific knockout mutations as well as
transgenics have been used extensively to address the cell-
autonomous function of interested gene and turns out to be
powerful genetic tool, particularly for mouse while nowadays
random genetic analysis is still not available.

btw, see if you can do me a favor and forward two papers from
Neuron. 1998 21:1243, and 1999 22:103 from Scott MP, to my
mbox [email protected] (one by one, pls:).

--
※ 来源:．The unknown SPACE bbs.mit.edu．[FROM: 128.118.]
发信人: Marble (小石头哥哥), 信区: Biology
标 题: Re: paper help/ call for MCBJC discussion
发信站: The unknown SPACE (Mon Feb 10 15:46:32 2003), 站内信件

NF1 can downregulate ras signaling. While upregulation of
P-MAPK was observed, it is speculated that ablation of NF1
leads to derepression of ras. The rationale is clear to me,
though you may talk about the figure per se. it also looks
fishy to me. i did not read the orginal paper on global Nf1
knockout, i guess they did similar experiment there.
and when i looked at fig3 j,k on the LCD screen of my laptop,
i was thinking, "what the heck are they showing me with two
black pannels?" then i turned the angle of the LCD and found
out there was indeed sth.
in this paper, actually they used several Cre strains to
generate conditional knockout (3 for neural crest). i guess
it is very hard to demonstrate the ablation of Nf1, thus they
use reporter strain to show the tissue-specificity, which i
do not like very much. virtually they did a lot of work, however,
as i am Mr. Peter Woodhead, unless you show me how much RNA
or protein is gone in a specific tissue, i could hardly buy
the whole story. however, they are lucky since the endothelia-
specific KO recapitulates most of the phenotype observed in
global KO. otherwise, this paper will not show up on Nat Genet.


【 在 assasin (冷血---何时能被加热？) 的大作中提到: 】
: The activated Ras pull-down experiment in Fig3. E is kind of fishy, isn't it?




--
※ 来源:．The unknown SPACE bbs.mit.edu．[FROM: 128.118.]