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I could use your help with the following. Feel free to answer one, or all... the more the better:

(1.) Hepatic glycogen storage diseases (GSD) are a group of rare genetic disorders in which glycogen cannot be metabolized to glucose in the liver, because of an enzyme deficiency. The introduction of continuous nocturnal glucose feeds and uncooked cornstarch has improved the prognosis for patients with GSD. In these patients, where does glucose get converted to pyruvate?
(a.) Nucleus
(b.) Mitochondria
(c.) Smooth ER
(d.) Cytosol

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Really? Ever hear of glycolysis....look it up
 
You have to approach this problem correctly. You know it's not the in the nucleus for sure. Now think where can there be something that can break down glucose? Not in the smooth ER because that is where Calcium storage is. So it's down to Mitochondria and Cytoplasm. Now we know that the main enzymes for breaking down glucose is in the cytosol already from cellular respiration and we know the mitochondria has transporters to take pyruvate in. So I'm thinking the answer is the Cytosol, but I'm not 100% sure. To back-up my answer, RBC's don't have mitochondrion and therefore can only go through glycolysis which means glycolysis happens in the cytosol and that is more than likely the answer.
 
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OP, it is the cytosol. You have to be careful with questions like that. The whole paragraph is fluff made to throw you off. And is it just me or do I only see one question here?
 
Whoa, the OP's been a member since 2002...

in before the :lock:.
 
Ya'll are hilarious...

Okay - anyone up for the challenge of 2 more?

(1.) The level of active mitotic CDK rises and falls during the cell cycle. Which of the following best explains why the levels of the active mitotic CDK rise?
(a.) Cyclin is degraded by APC, removing MPF inhibition
(b.) Active MPF tht already exists int he cell stimulates APC, which phosphorylates cyclin
(c.) New cyclin is produced, binds CDK, and then undergoes a series of phosphorylation and dephosphorylation reactions to gnerate active CDK
(d.) Checkpoint proteins trigger a MAP kinase cascade which activates transcription factors such as jun, that promote transcription of CDK protein.


(2.) The level of active mitotic CDK rises and falls during the cell cycle. Which of the follwing best explains why the levels of active mitotic CDK fall
(a.) Transcription of cylin stops after activation of p53
(b.) Polyubiquitination of APC triggers degradation of CDK
(c.) Active CDK stimulates a phosphatase that dephosphorylates CDK.
(d.) APC degrades securin, which allows separin to degrade cohesions holding sister chromatids together, which allows anaphase to begin
(e.) Active CDK activates anaphase promoting complex, causing polyubiquitination of cyclin.
 
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