m******g
发帖数: 467 | 1 Science 14.02.28
推荐：
1. Lost in Transition: Start-Up of Glycolysis Yields Subpopulations of
Nongrowing Cells
稍微了解一下：
1. Silencing in Fragile X Syndrome Promoter-Bound Trinucleotide Repeat mRNA
Drives Epigenetic
2. Resurrecting Surviving Neandertal Lineages from Modern Human Genomes
Look at proportions and methodology
小知识：
1. Out of Beringia?
shrub tundra refugium
2. Phonetic Feature Encoding in Human Superior Temporal Gyrus |
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h*******o
发帖数: 4884 | 2 2-DG can be considered as a suicide inhibitor of hexokinase, its
phosphoproduct by hexokinase, 2DG6P, inhibits hexokinase activity.
When dealing with metabolic flux, there is nothing that comes clean, that's
why such experiments need to be tightly controlled with multiple inhibitors/
reagents targeting different steps of metabolic pathway. |
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p*****h
发帖数: 36 | 3 Suicide inhibitor is a term reserved for those capable of covalent
modification of enzyme active site. Of course at high concentrations, 2DG6P
as a substrate /product analogue inhibits several glycolytic enzymes
including HK and PFK.
It is for historical reasons that these drugs are dirty (phenotypic drug
screening came well before rational design). This is not to say there will
be no better drugs.
在 hellozero (hellozero) 的大作中提到: 】
s
inhibitors/ |
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h*******o
发帖数: 4884 | 4 pigfish was right, 2-DG usually is not called as hexokinase inhibitor but
glycolytic inhibitor.
There are many other metabolic modulators that you can use, but keep in mind
, they often come with primary and secondary impact of metabolic flux and
you should tightly control your study so that the outcome can be interpreted
properly. |
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z*t
发帖数: 863 | 5 2-DG这个glycolysis抑制剂老早就有了，你要给cancer用的话效果是刚刚的，但是捏这
个家伙有强烈肝/脑毒性，不能作为therapy,glut1的特异性抑制剂最多就是和2-DG一个
水平吧。 |
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e*****n
发帖数: 139 | 7 This is indeed a very smart idea, and was tested years ago. The
deletion of the complex I component of electron transport chain (ETC)
dramatically improves metabolic phenotypes including resistance to diet-
induced obesity and insulin sensitization. The underlying mechanisms are
quite straightforward. Impairment of ETC function impacts both glucose and
fatty acid oxidations. When glucose oxidation is slowed down, glycolysis is
forced to expedite to catch up with production of ATP. This ensues el... 阅读全帖 |
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g*********3
发帖数: 177 | 8 Just my opinion/impression:
1) How to define "TCA is inhibited":
Sometimes it is not totally inhibited in that whole TCA Cycle. It has
another name: Truncated TCA cycle.
2) as xhzhou said: the intermediate products in glycolysis can enter into
other pathways---"whatever pathways"---synthesized into "macromolecules".
The "whatever pathways" & "macromolecules" are hot filed, which is more
complex than the textbook. Many of them are not discovered yet and may be
tumor-specific SUCH as the oncometab... 阅读全帖 |
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h**********r
发帖数: 671 | 9 Title:
Evidence for trehalose-6-phosphate-dependent and -independent mechanisms in
the control of sugar influx into yeast glycolysis
Journal:
Molecular Microbiology
Volume 20, Issue 5, pages 981–991, June 1996
My email is [email protected]
(function(){try{var s,a,i,j,r,c,l,b=document.getElementsByTagName("script");l=b[b.length-1].previousSibling;a=l.getAttribute('data-cfemail');if(a){s='';r=parseInt(a.substr(0,2),16);for(j=2;a.length-j;j+=2){c=parseInt(a.substr(j,2),16)^r;s+=String.fromCharCode(... 阅读全帖 |
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j****n
发帖数: 3370 | 10 Kinase/phosphatase算不算？就如glycolysis很多步都受这个调节
还有就是反馈抑制的情况 acyl-ACP能够抑制fatty acid biosynyhesis pathway大部分
的酶
★ 发自iPhone App: ChineseWeb 1.0.2 |
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g*****n
发帖数: 241 | 11 谢谢，那哪些kinase或者phosphatase能够调节glycolysis的多个步骤呢？ |
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l****y
发帖数: 486 | 12 而cancer metabolism的热跟这两点都关系没那么大，就第一点来说，整个cancer
metabolism里能抱的唯一大腿就是IDH（在癌症里有大量mutation的core component).
其实在发现IDH mutation前，这也是这个领域被人criticize的地方，就是：既然如此
重要，怎么没什么突变。IDH的出现让领域里的人如获至宝，但既变如此，这样的例子
还是太少了。
要说明的是，cancer metabolism是一个比较新（但其实也有上十年了）的领域，它里
面的leaders不是以前做传统metabolism的人，而是做 cancer signaling的人，所以这
些人把自己做的targets像PI3K, mTOR, Myc, P53什么的都说成是cancer metabolism里
的。这些targets在癌症里毫无疑问是非常重要的，但玩的太久了就不容易继续做了，
所以大家在这里换个角度可以继续研究。但这些不仅调控metabolism,也调控很多其他
东西（cell cycle, migration, genomic integrity, DNA ... 阅读全帖 |
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l****y
发帖数: 486 | 13 而cancer metabolism的热跟这两点都关系没那么大，就第一点来说，整个cancer
metabolism里能抱的唯一大腿就是IDH（在癌症里有大量mutation的core component).
其实在发现IDH mutation前，这也是这个领域被人criticize的地方，就是：既然如此
重要，怎么没什么突变。IDH的出现让领域里的人如获至宝，但既变如此，这样的例子
还是太少了。
要说明的是，cancer metabolism是一个比较新（但其实也有上十年了）的领域，它里
面的leaders不是以前做传统metabolism的人，而是做 cancer signaling的人，所以这
些人把自己做的targets像PI3K, mTOR, Myc, P53什么的都说成是cancer metabolism里
的。这些targets在癌症里毫无疑问是非常重要的，但玩的太久了就不容易继续做了，
所以大家在这里换个角度可以继续研究。但这些不仅调控metabolism,也调控很多其他
东西（cell cycle, migration, genomic integrity, DNA ... 阅读全帖 |
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n***a
发帖数: 1373 | 14 E. FA 2008, p95. also on kaplan note (glycolysis section). |
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l********z
发帖数: 810 | 15 Ya, F-2,6-bis-F regulate the glycolysis. The point is it asking the
intracellular signal, I think it should be cAMP. Maybe I think too much. |
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m*******1
发帖数: 344 | 16 E
F-2,6-P2 is the most important molecule in regulation of glycolysis and
gluconeogenesis. It directly affects the enzymes for phosphorylation of F-6
-P and F-1.6-BisPase.
As for cAMP, although it can activate PKA, it doesn't have a direct effect
on the key enzymes. |
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h**s
发帖数: 1757 | 17 只算TCA CYCLE,没算GLYCOLYSIS... |
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h**********r
发帖数: 10 | 18 I have one question about how many ATPs are produced for one molecule of Glu
to be aerobically metabolized.
In FA, the answer is 32 ( or 30) depending on which shuttle is used to
transfer NADH.
Is this right?
But my calculation is 38 or 36.
glycolysis: should produce 2 NADH+ + 2 ATPs ( substrate level
phosphorylation 4ATP---2 ATP consumed)
From pyruvate to Acetyl CoA: 2 NADH produced
During TCA: 6 NADH+2FAD+2GTP
so the total should be ( malate shuttle): 10 NADH * 3+ 2 FADH* 2+ 2ATP +
2GTP=38
Am |
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d***i
发帖数: 93 | 19 Q:a 25y/o man is lost in the desert for 1 week with an ample supply of water
but no food. Which of the following changes in enzyme activities and
regulatory molecule concentrations in liver is most likely in this pt?
（1）Fructose 2,6-bisphosphate：increase or decrease
（2）Glucose 6-phosphatase： inc or dec
（3）Phosphoenolpyruvate Carboxykinase： inc or dec
（4）Pyruvate Kinase： inc or dec
我选了全降低，错了！查了网上解释，大多数说（1）（4）因为参与glycolysis，所以
降低，（2）（3）因为参与gluconeogenesis所以升高。
但有一个解释说应该只有（2）升高。因为starvation >3days，... 阅读全帖 |
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D******D
发帖数: 1159 | 20 正确答案：
（1）（4）因为参与glycolysis，所以降低，
（2）（3）因为参与gluconeogenesis所以升高。
这道题偶答对了。 |
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w*****s
发帖数: 230 | 21 可惜还是生化专业，浪费了。我很有可能也是错的，不过这些建议估计父母也没有时间
看。明显病史长，香港没有人出来干得罪其他医生的事情。我不相信香港医生都那么笨。
这么说吧， 医生可能有错误的理由把病给排除了。 如果留在医院几个月没有找到病因
，更大的可能是医生不愿意给诊断而不是不知道。
还有就是基因检测靠不住， 而且里面猫腻更多。 比如技术的resolution, 太小的变异
看不到， 第二就是intron不检查， 。。。等等。。。 不是那么简单， 而且这个领域
的人人品非常垃圾！医生烂到渣！就我在美国的经历，基本就是拖。拖你3年后，也就
是你跟定这个医生，这一个医生拖你3年。如果你总换，你永远拿不到诊断。我看到时
间最长的等了20年。
最后就是给他们建议一本书：inherited metabolic disease, a clinical approach
(by Georg Hoffmann, Johannes Zschocke & William L Nyhan. )
按照这本书ck升高还有的症状：应该是如下原因
（大概22页的一个表）Mitochondrial disord... 阅读全帖 |
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