Final Flashcards
Describe the path of transmembrane proteins from synthesis to destination.
Protein synthesized in ER upon recognition of N terminal ER sequence.
- They will be folded correctly in the ER by chaperones
- modified with SS bonds and glycosylation (as needed)
- Then transported to the golgi for further modifications and processing
- Release of proteins from the cell via exocytosis
What happens if there is a cystic fibrosis protein
Protein remains in the ER because the channel is misfolded, degrading the protein inside the ER
What happens to protein that are not folded correctly after synthesis in the ER?
They will retain in the ER and eventually moved to the cytosol and degraded.
Describe the transport of protein into the nucleus. How is ran protein involved?
- Nuclear Transport Receptor binds to the signal sequence of protein and transport it to the nucleus.
- Receptor dissociates from the cargo and binds to Ran GTP
- Receptor exits the nucleus and Ran GTP is hydrolyzed to Ran GDP, dissociating the GDP from the receptor
- Cycle Repeat
What type of protein modification happens in the ER and Golgi?
In the ER, glycosylation and disulfide bond modification
In the Golgi, proteins are sorted and undergo further glycosylation if needed
Will a protein ALWAYS be transported to the Golgi after it has been in the ER?
Not all proteins move on to the golgi. Proteins with C terminal ER retention signal – stay in the ER,
Define Phagocytosis and Pinocytosis
Phagocytosis: ingesting large molecule via large vesicles
Pinocytosis: Ingestion of fluid and small molecules via small vesicles
What is the function of clathrin in cells?
Clathrin coats the outside of transport vesicles to shapes the membrane into a bud and helps capture molecules for transport
What is the difference between early endosome, late endosome and lysosome?
Early endosomes – vesicles just beneath plasma membrane
Late endosomes – vesicles closer to the nucleus
Lysosome- collection of enzyme that degrade biological polymers
Describe the series of events that leads to muscle contraction upon Ca2+ release from the sarcoplasmic reticulum
When calcium levels rise, troponin shifts the position of tropomyosin so that myosin can bind to actin, contracting it. If troponin is deleted, tropomyosin is always bound to actin, preventing myosin from binding to actin – muscle cannot contract
What is the likely effect on muscle contraction if the actin binding site on tropomyosin is
mutated so it no longer binds actin? Explain.
Muscle will not be able to relax since there is nothing stopping it from binding to actin. Muscle contraction is not coupled to calcium dependent signals
What is the basic function of a kinesin?
Kinesin is a motor protein that binds microtubules and moves cargo – vesicles, organelles along the microtubule
How is it different from the function of dynein?
Kinesin – will move cargo from the minus end to the plus end of the microtubule
Dynein is another motor protein that moves cargo from plus end to minus end
Define centromere, centriole, centrosome. Which of these is not a component of the cytoskeleton?
Centromere: Center of chromosome
Centrosome: specialized organizing centers from which microtubules form.
Centriole: Center of Centrosome
Centromere is not a component of the cytoskeleton
Describe the 5 different types of signaling, give examples of signals for each. which signal is the most suitable when the message needs to be broadcasted broadly throughout the organism?
Endocrine – insulin
Paracrine - histamine
Autocrine – any of these if cell has receptors for them
Neuronal – GABA, glutamate
Contact-dependent – delta-notch
What determines the response evoked in a cell to a specific signal?
The unique combination between the signaling molecule and the type of receptor it interacts with, in combination with intracellular signals that converge on the same pathway
Name 3 types of cell surface receptors we discussed in class. Is this the only type of signaling (via cell surface receptors)?
Ligand gated ion channels, GPCRs, RTKs
Signaling can also be done via intracellular receptors (steroid hormones and nuclear receptors), or enzymes (NO)
What is cholera toxin
acts on Gαs – inhibits GTP hydrolysis – constitutively active
What is similar between nitroglycerin and sildenafil (the active ingredient in Viagra)?
Both modulate the effect of nitric oxide gas (NO) causing dilation of smooth muscle
Calcium activates Nos, the enzyme that generates nitric oxide gas
NO activates guanylyl cyclase to make cyclic GMP (cGMP) which ultimately causes relaxation of the smooth muscle allowing more blood to flow through the vessels
Sildenafil acts on the enzyme phosphodiesterase that breaks down cGMP, thus prolonging its effect
Calcium activates NOS. NOS generate NO which binds to guanylyl cyclase to make cGMP. This cause relaxation of smooth muscle.
Sildenafil enhances NO, promoting relaxation
What is the difference between paracrine and autocrine signaling?
In autocrine signaling, a cell signals to itself, releasing a ligand that binds to receptors on its own surface. Paracrine cannot do this.
What are second messengers? What are examples?
molecules that are activated following receptor activation
cAMP, calcium, IP3, DAG
What is the advantage for utilizing second messengers in a signaling pathway?
The advantage of utilizing second messengers is to be able to amplify
Or relay the signal to multiple different targets, intersect with other signaling pathways
Ex:
IP3 relay signal to AKT
cAMP relay signal to promote glyogen breakdown
Calcium relay signal that leads to cGMP
DAG relay signal to PKC
What is the pathway that activates PKA?
GPCR -> Gprotein alpha s -> adenylyl cyclase -> cAMP -> PKA
What is the pathway that activates PKC from GPCR
GPCR -> G protein alpha q -> phospholipase C -> DAG -> PKC
