I like how that's the structure of caffeine in the bottom-left corner.
What, no Krikkit references? Come on, people!
it's called an "optimistic history" for a reason.
i'm glad it's got a nice, ominous, science fiction sounding name so we won't have to nickname it when it inevitably turns against us.
Nooo, they say gamers solved it because they solved it...in a game. Get it? They were playing a game to solve it, therefore they are gamers. Processing power had nothing to do with this, you're thinking of a distributed computing effort like Folding@Home.
Computers would have to try every possibility of conformations, while human intuition can say "this looks like it might work, I'll try it and see." It's a surprisingly powerful tool.
Source: A college degree in Molecular Biology and Biochemistry.
Source: A college degree in Molecular Biology and Biochemistry.
How about next time you send out emails with picture links embedded (the Deus Ex easter eggs one) you don't link an image titled "dildos.jpg." I got to have an interesting talk with my boss about that one. #kotakueditorialboard
You use it for rappels on the way down. Tie a releasable knot for a rappel and you can use it for multiple raps.
On routes like this, cameramen are placed at certain spots. Mostly lower to the ground, where they can rappel down easily enough. That's why the top shots (minus the last one, which was probably a photographer flown up) are all aerial.
That helmet already saved his life once on an earlier fall. He fell 200 feet a couple years ago and shattered his helmet, but he was mostly uninjured.
My thoughts exactly. I mean...MONKEYS.
The difference seems to be that our plans include MUCH more voice than the common plans you listed there. 2 hours is NOTHING compared to the 5000 minute or unlimited talk plans commonly found here. Priorities seem to be placed differently.
Ah, so if certain drugs stop replication downstream of Ras, then I can see how that would inactivate the pathway. I wonder if maybe some of the blocking of ligation is occurring with second messengers inside the cell and downstream of Ras?
As far as I know the receptor is not capable of being constitutively active, but I could be wrong on that. I know Ras losing its GTPase activity is very common in a lot of cancers, but I've never heard of a receptor being permanently active (not to say it can't or hasn't happened, my knowledge on this is limited to what my textbooks tell me).
I appreciate the response, and I liked your explanation as to why blocking ligation may be helpful even if Ras is already activated. I loved seeing this post pop up, as it was something I had just studied in a Signal Transduction course, so it was cool to see some sort of practical application for all the theory I had just learned. I'm actually hoping to go into research (majoring in Molecular/cellular biology) and cogent, concise explanations like these are much appreciated, as I'm sure you know textbooks have a nasty habit of being a bit wordy...
As far as I know the receptor is not capable of being constitutively active, but I could be wrong on that. I know Ras losing its GTPase activity is very common in a lot of cancers, but I've never heard of a receptor being permanently active (not to say it can't or hasn't happened, my knowledge on this is limited to what my textbooks tell me).
I appreciate the response, and I liked your explanation as to why blocking ligation may be helpful even if Ras is already activated. I loved seeing this post pop up, as it was something I had just studied in a Signal Transduction course, so it was cool to see some sort of practical application for all the theory I had just learned. I'm actually hoping to go into research (majoring in Molecular/cellular biology) and cogent, concise explanations like these are much appreciated, as I'm sure you know textbooks have a nasty habit of being a bit wordy...
i like how the front is positioned so a minor crash will chop your head clean off.
Kaiser-Machead is Zombie Osama Bin Laden, returned from the watery depths to haunt us once again.
Vernor Vinge!!!!!!!!!!! gleeeeeeee
<3
<3
Congratulations, you win the internet.
Well technically that's not just one pathway. It's the EGFR group of pathways, but there is a lot of crosstalk between them so a ligand binding an RTK receptor and causing cross-phosphorylation might be one pathway, but there may be several other types of receptors (I at least see G-protein coupled receptors also activated by this ligand just from a quick glance) activated. So in essence, this is actually a lot of different pathways, it's just all the pathways begun by the binding of the EGFR ligand.
"The way this process works is that first, a pathway is identified that is working abnormally in the malignant cell. Most often these days, the pathways involve the epidermal growth factor receptors (EGFR). EGFR is a huge family of cell surface receptors that bind a ligand (a molecule in the blood that fits like a lock and key) which usually causes two receptors to join up (dimerize) and activate a signaling pathway. In a cancer, these processes can turn on without ligand binding or without dimerization; or once they turn on, they don't turn off, or there are too many of the receptors on the cell surface (overexpression). There are probably other ways the process can go wrong, too.
However, now that you have identified that this usually normal process as abnormal in the cancer cells, you can attack it. You can design a molecule (literally design the molecule with a computer's help just like in Neal Stephenson's The Diamond Age) that will either grab the ligand to keep it away from the receptor, block the receptor, prevent dimerization, or block the process downstream. Since some part of the malignant process is the result of mutation, it is theoretically possible to design a drug that will only affect the cancer cells, not normal ones. This is the fabled "magic bullet.""
Correct me if I'm wrong, but the Ras mutation removes its intrinsic GTPase activity, thus making it constitutively active. So even if ligation is blocked, all it would take is a different pathway activating Ras or it being activated beforehand and not turning off, right? So even if ligation is stopped, wouldn't it essentially be too little too late in the case of a Ras mutation?
However, now that you have identified that this usually normal process as abnormal in the cancer cells, you can attack it. You can design a molecule (literally design the molecule with a computer's help just like in Neal Stephenson's The Diamond Age) that will either grab the ligand to keep it away from the receptor, block the receptor, prevent dimerization, or block the process downstream. Since some part of the malignant process is the result of mutation, it is theoretically possible to design a drug that will only affect the cancer cells, not normal ones. This is the fabled "magic bullet.""
Correct me if I'm wrong, but the Ras mutation removes its intrinsic GTPase activity, thus making it constitutively active. So even if ligation is blocked, all it would take is a different pathway activating Ras or it being activated beforehand and not turning off, right? So even if ligation is stopped, wouldn't it essentially be too little too late in the case of a Ras mutation?
