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o DNA sites that RNApolymerase binds to at which transcription begins. The promoter is justupstream (closer to 5’ end) to the point of transcription initiation.
o : DNA sites at or nearthe promoter that bind repressors. These need to be close to the -10 and -35regions, which bind sigma factors, so that the binding of repressors to theoperator prevent binding of the sigma factors.
Operons. Inprokaryotes, the regulation of gene expression is controlled at the level oftranscription since translation and transcription occur simultaneously sincethere is no nucleus separating translation machinery from transcription.
chromatin structure (hetero vseu)
-Hyperacetylation(by HAC) of histones is associated with active transcription of genes-Hypoacetlayion (by HDAC) isassociated with inactive transcription of genes
Enhancers(increase rate of transcription) and Silencers (decrease rate of transcription). Can be located far up or downstream to transcription site (unnlike basal promoter).
Levelsof transcriptional regulation
-Primaryresponse: no new protein synthesis is necessary for induction of transcription.It is the initiation of transcription to create RNA
-Secondaryresponse: new protein synthesis is necessary for induction of transcription.This protein is generated in the primary response.
-Alternative Promoters: use of different promoters for the same gene, often depending on cell type (ex glucokinase expression in the pancreas vs. liver.
Abase within the mRNA strand is changed so as to create a stop codon. This allows for the premature termination of proteinsynthesis. Example: ApoB100 vs. ApoB48
Thischanges the carboxyl terminus of protein. This is how lymphocytes are able tocode some membrane bound antibodies (leaving a hydrophobic tail on the protein)or cleave off the sequence coding for the tail so that the protein ishydrophilic, as in the case of secretory antibody.
The cell keeps levels of Dihydroxyacetone really huge, and thenkeeps drawing off the G3P to continue glycolysis, causing the whole process towork. By making a low conc of G3P in the cell, it makes the dihydroxyacetonewant to change into G3P, so it happens instead of going in reverse. Its lechatelier's principle in action that forces the process forward.
This is a principle that the cell uses all the time in pathways to keep them going forward.
The lacticacid cycle is important b/c it helps replenish the NAD+ that we need in caseoxygen levels get super low. If o2 levels are low then the cell runs out ofNAD+ and then you're really screwed. It like having currency that isn'taccepted anymore
Pyruvate dehydrogenase catalyzes the rxn that turns pyruvate and uses NADH to do so, freeing up NAD+'s
Receptortyrosine kinase - the ligand actually forces a dimerization of two subunits.They then come together and then it autophosphorylates (phosphorylates itself), this then causes Ras to become activated by certain means, and so on and soforth MEK1/2 ERK1/2, fos & jun become the TFs that bind DNA and increase transcription. I have a cool youtube video of it saved online.
G protein- 3 subunits. Alpha subunit can move away from the other 2 subunits.
Alphasubunit is itself an enzyme, and binds GTP to become active, and in its restingstate is bound by GDP. This affinity for Guanosine nucleotides earned it its name. When a G-protein coupled receptor (It's always a 7-pass integral membrane protein, and there aremany receptors for many diff. things) binds it's specific ligand, it activates the g-protein to do its thing by swapping its GDP for a new energized GTP.
After activation, a G-protein canbasically turn itself off! It uses its GTPase to turn its GTP into GDP and thatmeans "off"
Goes backto the the receptor to see if its still on or nto, and IF IT IS, it will gothrough another cycle of this madness. This contributes to the maintenance ofsensitivity of the system
Basically,the duration of the calcium spikes are what is read by the cell and the different frequency of the spikes tells the cell to do different things!
OIL -oxidize is (Carbon) losing e-s
RIG -reduction is (carbon) gaining e-s
The pentose phosphate pathway uses NADP+ instead of NAD+. The twomoleules are very similar and the P just sets it apart for this job ofbiosynthesis, while the energy creation stuff is for NAD+. Its likecreating two separate pools and keepthing them separate so you can havestockpiles for both
So, DHAP,one of the products of aldolase in glycolysis, can be snatched (remember howthe cell has a huge pool of it?) and turned into this glycerol-3-phosphate (notto be confused with G3P!!!) via a cytosolic G3PDH (G stands for Glycerol, notglyceraldehyde). It can then cross the outer membrane of the mito. and drop its e's off at themitochondrial G3PDH nestled in the inner mito membrane,, which gives them to Q which gives them to complex 3. G3PDH is now DHAP again.
- b/c thecell needs NRG somehow, it uses glycolysis to get R done, and in order to keepdoing glycolysis once it runs out of NAD+ it has to make NAD+ by making lactate. So anerobic resp. sets in.
- Fatty acid metabolism is stopped as well. If the fatty acids aren't burned in the mito, then theyare just stored away as triglcerides (you can get a fatty liver from this)
The problem is, the CELL TRIES TO COMPENSATE FOR IT by increasing ETC rate and metabolism. This can lead to overheating and death if too severe.
The namingof these came from the fact that when they named them, they were named based ondensity centrifugation. Also note that the more dense ones have high % protein,since lipids are less dense than proteins!
- doing thecitrate thing not only produces an Acetyl-CoA, but it also produces an NADPHthat will be needed later to make the fatty acid.
- ALSO: thePDC is only found in the mitochondria, so you couldn't just take pyruvate andturn it into acetyl-CoA in the cytosol if you wanted.
- ALSO:acetylCoa is actually a HUGE molecule with 4 negative charges, so it will nevercross the mito membrane alone. That's another reason
Regulation of Glycolysis
-Glucagon->cAMP->PKA-> phosphorlylation of PFK-2/FBPase-2 complexinhbits PFK-2 and activates FBPase-2 causing levels of F2,6BP to decrease
Consequences oflower F26BP: gluconeogenisisactivated and glycolysis inhbited (slowing)
Regulation of CAC
-regulation of alpha-ketoglutarate dehydrogenase; inhibited by succinyl-CoAand NADH; stimulated by Ca2+
citratesynthase is inhib by citrate (IsoDH pulls nor.)
malate/oxaloacetateeq :NADH/NAD+ decreases, ratio of OAA/malate increases
Dephosphorylated = active
-PDC Kinases and PDC phosphotases – control amount of inactive and active form ofenzyme
-you can also control activity bw kinase and phosphotase
ADP has negative effect of kinase activity (thus keeps PDH in moreactive form)
Ca2+ has positive affect on phosphatase activity
-fatty acids = precursors of ketone bodies in the liver. Factors governing fatmobilization affect ketogenesis
-duringfasting, fat mobil. is enhanced and ketogenesis is increased
-duringfasting, blood glucose levels begin to fall, and glucagons levels areelevated
--in liver, beta ox of FA produces NADH and ATP, andacetyl CoA If enoughacetylCoA, PDH = inhibited
-OAA conc. reduced since flow in rev. dir. for gluc.
If youstart with an odd-chain fatty acid then you get left with a 3 C final product(propionyl CoA) instead of acetyl-CoA. But this can be dealt with by turning itinto Succinyl CoA and sending it off to TCA land.
Whenever the enoyl isomerase operates, he takes the acyl-CoA dehydrogenase's job (its usual job isto make the double bond during the first step) so less energy is gained b/c that process usuallyresults in an FADH2 being formed. So that FADH2 is never formed if enoyl CoAisomerase is used. This ends up being a difference of 3 ATP.
Chronic consumption of ethanol leads to more MEOS out thereto metabolize stuff.
Also, since theMEOS doesn't ONLY do ethanol, it does other drugs also. However, if you takedrugs AND ethanol at the same time, they both compete for the same enzymes, soboth stay in the body longer!
PG_ is the nomenclature
PG stands for prostaglandin
Letterafter = certain variety of prostaglandin. Most often, these different varieties are tissue specific
The different varieties are based on different groups coming off of the ring (the "head")
What do cells do with the LDL's they take up?
Why arefamilial ligand defective apoB-100 sufferers less screwed than familialhypercholesterolemia pateints?.
Theproblem here is that they don't have a functional adaptor protein for the LDLreceptor to help it cluster in the coated pits. This only happens in the liver,however!
Why doesit only affect the liver?
There is ahomolog of this protein that peripheral tissues have but liver doesn't. AKALIVER DOESN"T CARRY A SPARE TIRE FOR THIS ADAPTOR PROTEIN.
There are proteins (ABCG5 and ) that are pumps that are able to pump cholesterol out of the live into bile,or out of enterocytes back into lumen. They excrete cholesterol out of the body. In this disease, these proteins are jacked, so cholesterol isn't excreted from the body as much.
This alsoapplies to plant sterols, which is why these people turn green, the plantsterols build up all sorts b/c they can't be exported.