Cell Cycle, Cell Signaling, and Disease Explained Clearly
01
September

By Adem Lewis / in , , , , , , , , , , , , , , , , , , , , , , , , /


okay so we’ve talked today about
cell phones and text messaging I’m just kidding we’re actually talking about the
cell cycle and messaging within the cell and how it relates to current disease
and treatments for more lectures like this please check us out at Med cram
comm what I wanted to talk about it kind of goes back a little bit to high school
biology but this is really cool because we’re actually starting to see some of
our discoveries that we’ve made years ago come to fruition today so let me
draw for you the cell cycle so if you remember from high school biology
there’s a cycle where the cell reproduces itself through the process of
mitosis mitosis isn’t the only thing that happens it’s just part of it you
remember there is prophase metaphase anaphase telophase well that has to do
with mitosis so this is phase M okay but that’s kind of the last thing that
happens usually what happens is the cell stays in either g0 so that would be the
pre synthetic phase or it goes into g1 now g1 is where it’s preparing to divide
and the first thing that it needs to do before it does divide is it needs to
replicate its DNA and that’s called the S phase S stands for synthetic and
that’s where you have chromosome duplication it’s very time consuming
very energy consuming so once it actually reproduces its DNA then it’s
then going to go into a pre mitotic phase known as g2 and it will continue
to grow until it’s ready to actually go through the division process so let’s
follow this around here you have a cell it makes a decision to go through with
dividing it’s got to reproduce all of its chromosomes all of its DNA then it’s
got to grow some more and then finally divide and this could keep going in the
case cancer or it could exit and stay as a
cell in g0 so what’s really interesting about this is that the body regulates
this pretty well normally and there’s a restriction point right here right
before the S phase okay so this is a restriction point and it makes sense
because you don’t want to go through this takes a lot of energy if things are
not right okay and this is regulated by cyclones which are proteins that make
sure that it’s ready to go through with replication so this restriction point if
it finds that it’s not quite perfect or not quite ready it will exit out of the
system and you will get something called senescence okay basically it’s
programmed death which causes some inflammation for instance if there’s
oxidative stress if there is cellular damage and it detects that so before it
copies it it’s going to say you know what the cell is not ready to divide we
should not be dividing the cell we’re going to replicate errors it’s not a
good idea so it exits the cell right here before the S phase this is called
the restriction point and it’s cyclones which mediate that okay now let’s say
that everything’s good and it goes through the S phase the next thing
that’s going to happen is there is another checkpoint right before it goes
through mitosis and actually divides so in other words there is another
checkpoint over here and it will look to make sure that the DNA was reproduced
correctly so if it wasn’t reproduced correctly
then it’ll say you know what we need to just involute and die and that’s called
a proptosis now a pitocin is very important because a pitocin give
information okay but you could also get replicative senescence which does cause
inflammation okay now there are a couple of other terms that you may not have
heard of one of them is Auto Fidji this is where
the cell starts to break down itself and starts eating itself it’s like a
catabolism state another word that you may not have heard is necroptosis okay
this is where the cell dies and it uses something called an RI P which is kind
of cute rest in peace but it’s an RI P kinase and this also can cause
inflammation now there’s another thing called F ro cytosis and this is pretty
cool because here you have phagocytosis with leukocytes that actually eat up the
trash and the cellular debris and it reduces autoimmunity and it reduces
inflammation so that’s good okay so this is generally the cell cycle that we’re
talking about there’s a number of things that can happen to cells in the cell
cycle and the purpose of all of this is to make sure that only good cells
reproduce and bad cells stop reproducing or they die and this is to prevent
cancer when you go through the cell cycle one of the things that happens
when you do this synthetic phase is you lose something called telomeres
telomeres are the ends at the end of the DNA so let’s say this line here was the
DNA there would be little telomeres at the end because every single time you
reproduce or duplicate a chromosome you don’t reproduce the whole thing you get
a part of it cut off and so there is something called telomerase –is which
add on to the end well in certain cases you don’t have these enzymes because
there’s mutations in them and these enzymes are things called te R T and T e
rc so turts and turks and they found that mutations in these
have been found in patients with idiopathic pulmonary fibrosis and also
COPD in fact idiopathic ptosis have mutations in both tert and
Turk whereas COPD just has mutations in Turk
so once again we see the cellular basis here of disease now the other thing I
want to mention is this restriction point and for that matter this one too
in fact all of this is regulated very strictly by receptors and we’re going to
talk about a specific receptor called an intrinsic tyrosine kinase this intrinsic
tyrosine kinase phosphorylates enzymes which allows transcripts on the DNA to
work and these intrinsic tyrosine kinases
can be activated by different receptors and we’re going to talk about those
receptors next because if we can eliminate the tyrosine kinase from
signaling this to go through we can potentially take cancer and arrest it in
its tracks so let’s talk about that because that’s
pretty important okay so there’s four types of receptors that we’re going to
talk about there are receptors with intrinsic tyrosine kinase activity and
then we have receptors that are lacking tyrosine kinase activity and then we
have G proteins and steroid let’s talk about these receptors with intrinsic
tyrosine kinase activity so these are receptors that directly control the
entry of cells into the cell cycle so they directly control cell cycle you can
see why this would be a target for cancer treatments okay so what are the
type of receptors that we’re talking about there is the epidermal growth
factor there is the platelet-derived growth factor there is the vascular
endothelial growth factor fibrosis growth factor
and tgf-beta so these are all receptors on the cell surface that interact
directly with a intrinsic tyrosine kinase which will directly control cell
cycles so the purpose of this is to find the receptors for all of these and to
block it and if we can block it then potentially we can prevent cancer from
forming so the epidermal growth factor receptor can be blocked by medications
for instance get fit in nib you’ll notice that they all end in B’s another
one is ER l OT ini be another one is AF a TI n ib so these are all receptor
blockers okay platelet derived growth factor veg F R and FG f R and things of
that nature these can be blocked at least these
three right here can be blocked by something called in the tid a nib and
that was FDA approved back in 2014 for the treatment of idiopathic pulmonary
fibrosis so IPF and it kind of slows down the progression again this is
utilizing through a tyrosine kinase receptor blocker now real quick cells
that lack tyrosine kinase would be receptors like il-2 three and a fair on
gamma and they actually use something called a jak kinase and then they signal
to the cell using something called stats these are second messenger things that
go into the nucleus and transcribe from there you may recall that G proteins use
gtp and they use cyclic a.m. P as second messengers and then finally steroid
hormones our steroids of course that kind of looked like vitamin D kind of
drawing this schematically here without spending too
much time looks like a steroid and it kind of cuts right through into the
nucleus of the cell without any receptors and it does transcription
perhaps a better picture would be like something like this okay so kind of like
a vitamin D or cholesterol analogue okay so this explained a little bit about
cell cycling let’s talk about cell mediated immunity and helper T cells and
things of that nature in the next lecture hi I’m dr. Rajesh well we’re
excited to announce the launch of med cram comm you know over the past four
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4 thoughts on “Cell Cycle, Cell Signaling, and Disease Explained Clearly

  1. Thanks for watching!
    Over 100 hours of free medical videos by Dr. Seheult at www.MedCram.com
    Topics include cardiology, critical care, pharmacology, pulmonology, G.I., infectious disease, acid/base, hematology, radiology, board questions, and more.

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