So now that we've covered all of the bio signaling pathways that we're going to cover in our clutch prep biochemistry course, we're going to move on and talk about signaling defects and cancer. And so defects and bio signaling pathways can cause the bio signaling pathways to fail to elicit the cell response, and that will thus lead to disease. And so cancer is a very specific type of disease that's characterized by uncontrollable and inappropriate cell growth, and it is also associated with signaling defects. And so, in our next lesson video, we're going to introduce the types of genes that control cell growth so that we can take a better look at understanding how cancer can develop. And so I'll see you guys in our next video.
Signaling Defects & Cancer
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So in this video we're going to introduce the two types of genes that regulate cell growth. And so again, in a healthy and normal cell, really, there are two types of genes that regulate cell growth that we have number down below number one and number two, and so the first one are going to be proto uncle jeans. Now, proto oncogenes are genes themselves that provide signals that promote appropriate cell division. And so proto oncogenes pretty much act like the green light for cell division, allowing cell division to proceed again at a normal on healthy, appropriate rate. And so if we take a look at our image down below at the proto oncogene, noticed that we're pretty much saying here that it acts like the green light for cell division, allowing cell division to proceed at a normal and healthy rate at an appropriate rate. And so proto oncogenes are pretty much acting like the gas pedal for cell division. And so a classic example of a proto oncogene is the gene that encodes the monem Eric G protein Wrasse, which recall wrasse, was found in the insulin rtk signaling pathway as a growth hormone and So when the wrasse G protein is active, it will appropriately and healthfully and normally stimulate or promote cell growth. And so wrasse is a classic example of a proto oncogene. Now the second type of gene that is again found in healthy and normal cells that regulate cell growth are these tumor suppressor genes. And so the tumor suppressor genes, as their name implies air going to be genes that provide signals that suppress or inhibit cell division. And so tumor suppressor genes pretty much act like the red light for cell division inhibiting cell division acting like the bricks for cell division. And so if we take a look at our image down below, notice that we're showing you that tumor suppressors pretty much act like the red light for cell division to again stop or inhibit cell division from proceeding. And so pretty much tumor suppressors act like the brakes to cell division, inhibiting cell division again at a healthy and normal rate of inhibition. And so a classic example of tumor suppressor genes are the genes that encode the phosphate tastes is that we talked about in our previous lesson videos for bio signaling and so recall that phosphate tastes are enzymes that remove phosphate groups, and so they reverse the kindness activity. And so phosphate cases we have seen are involved with the termination or the inhibition of a signal. And so foster cases in the insulin rtk signaling pathway as a growth hormone would be used to inhibit the signal and inhibit cell growth again, as we just indicated here. And so really, this is the end to our introduction to the types of genes regulating cell growth and again in healthy, normal cells. There are proto oncogenes, which act as the green light for cell division and tumor suppressor genes, which act as the red light for cell division. And so this here concludes this video, and I'll see you guys in our next one.
Signaling Defects & Cancer
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In this video, we're going to introduce how unca genes, which are different than the proto oncogene that we introduced in our last awesome video and mutated tumor suppressor genes actually promote cancer. And so although the proto oncogenes that we talked about in our last lesson video are healthy, normal and essential, they're also really susceptible to mutations that generate uncle jeans. And so again, Anka genes are different than proto unca jeans proto oncogenes again our normal, healthy and essential, whereas UNCA jeans, on the other hand, are bad because they are again mutated genes that are going to promote unrestrained cell growth or essentially, Anka genes are mutated genes that promote cancer. And so these are bad genes that we do not want. And so the proto oncogene encoding, the Monem Eric G protein called wrasse, is actually one of the most commonly mutated in human cancer tumors. And so when the proto oncogene and coding wrasse is mutated, it becomes an oncogene, and so notice down below. Over here on the left hand side and image number one, we're showing you how unca genes can lead to cancer development, and over here on the right hand, side image. An image number two. We're showing you how mutated tumor suppressor genes can lead to cancer development. And so we'll start off with image number one here. And so, of course, the number one up above in the text corresponds with the number one down below in the image. And so really, what we're showing you is that the most common mutation and cancer tumors is the loss of wrasse is intrinsic GTP, ace activity and recall from our previous lesson videos when we covered insulin Arctic bio signaling, uh, that the GTP ace activity of a G protein will cleave the high energy active GTP into the low energy inactive G D P. So the GPS activity is used to inactivate the G protein. However, if we have a mutation that leads to the loss of the GPS activity, then the G protein will not be able to inactivate itself. And so that means it's going to keep rass in the active state. And so if wrasse is in the act of state, then that means that it's going to overstimulate or over promote, uh, cell growth so that you get unrestrained cell growth and cancer and So if we take a look at our image number one down below noticed that at the top here, we're showing you are like an binding to the receptor, and that is going to lead to a Siris of signal transaction events that is ultimately going to make its way into the nucleus to affect transcription factors that will affect the transcription of very particular genes in our DNA. Now notice here we're showing you an oncogene, and it's an oncogene, which means that it has a mutation in it. And so when the transcription factors, uh, promote the transcription of this oncogene here, it's going to lead to the mutated wrasse protein. And this mutated rats protein is going to have a loss of intrinsic GTP ace activity, which means that it will not be able to inactivate itself and will therefore remain in the active state. And so mutated rats we know is going to overstimulate cell growth and lead to the development of cancer. Okay, now, over here in image number two, really? What? We're showing us how mutations and tumor suppressor genes such as phosphate aces can also lead to cancer development. And so, if we take a look at our image down below, over here in image number to notice again that we're showing you the lie again, binding to the receptor here in the membrane leading to a Siris of signal transaction events that makes its way into the nucleus to activate specific transcription factors and notice here that the DNA gene that we're showing you here is for a mutated tumor suppressor gene. And so, normally, we know that tumor suppressor genes are again healthy and normal and essential, and they're used as breaks to help inhibit the cell growth. However, if you have a mutated tumor suppressor gene, that means that you have mutated breaks, basically broken brakes. And so when these transcription factors essentially, uh, promote the transcription of the mutated tumor suppressor gene, it's going to lead to a mutated phosphate taste, which is this yellow protein that we're showing you here. And of course, the mutated phosphate taste will not be ableto work or function properly, which means that it will not be able to remove phosphate groups and reverse the activity of phosphate taste is so it will be unable to inhibit cell growth, and therefore it's going to promote cancer. It's almost like having broken brakes. And if you have broken breaks that will not stop cell growth, then that means that cell growth is going to be promoted and cancer will be promoted. And so this year concludes our lesson on how Anca jeans and mutated to miss suppressor genes promote cancer. And so, as we move forward in our course, will be able to get some practice applying these concepts, so I'll see you guys in our next video.
Is there a difference between oncogenes and tumor suppressor genes?
Yes, oncogenes are genes that can cause cancer when they become mutated to become proto-oncogenes, whereas tumor suppressor genes play no role in cancer.
Yes, oncogenes prevent cancer from forming unless they are mutated to become proto-oncogenes, whereas tumor suppressor genes stimulate the formation of cancer even in the absence of mutation.
No, oncogenes and tumor suppressor genes both stimulate the development of cancer, even in the absence of their becoming mutated.
Yes, oncogenes are mutated versions of genes that promote abnormal cell division (such as mutated Ras), whereas tumor suppressor genes are genes that normally inhibit cell division.
No, since both types of genes contribute to the development of cancer, there is no difference between them.
The protein product of the Ras oncogene is a mutated Ras protein. All of the following would be true EXCEPT:
The Ras protein is a G-protein and functions as an internal clock.
G-proteins have evolved to stay active for a certain length of time.
Ras protein is active in cell growth and division.
Ras can mutate so that it is less active as a GTPase.
A less active GTPase would mean less stimulation of the MAP kinase pathway.
How does a proto-oncogene differ from an oncogene?
Proto-oncogenes code for proteins that regulate expression of structural genes; oncogenes code for nucleic acids involved in cell division.
Proto-oncogenes control normal cell division; oncogenes contribute to the development of cancer.
When oncogenes become damaged, they become proto-oncogenes.