Cell Signaling/Cell Cycle

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Author:
lace.granatelli
ID:
120797
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Cell Signaling/Cell Cycle
Updated:
2011-12-10 03:30:38
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Cell Signaling cell Cycle
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CELL SIGNALING
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  1. What are the different types of signaling molecules and how does a cell respond to these signals
    • Endocrine: signal in blood = hormones = long
    • distance

    • Paracrine: signal diffuses short distances
    • = adjacent surrounding cells

    • Neuronal: signal diffuses short distances =
    • could be short or long = used neurotransmitter

    • (axons are long but the synaptic cleft is
    • short)

    • Direct contact: signal diffused a very! Close
    • distance = most intimate = no secreted molecule
  2. Describe how endocrine cell signals work
    Endocrine cell release signal --> signal goes to blood --> carried through the body --> respond
  3. What contact does paracrine have? uses what as signal molecules?
    • Paracrine is direct contact
    • Signal molecules = lcaol mediators (short half life)
  4. Cell conversation is know an what?
    • Transduction:
    • relay molecules, send messages, amply it, and send it out
    • Transduction begins when receptor protein on target cell recieves the extracelluar message and coverts to intracellular

    Signal may lead to variation, cell crawling, get rid of pathogens, different potential responses
  5. Describe the basic steps of cell communication.
    Receptor --> Transduction --> Response
  6. Describe paracrine
    Paracrine: signal diffuses short distances= adjacent surrounding cells
  7. What is integrating of cells?
    Integrating: combination of signals tells the cell what to do at that time
  8. What won't a cell respond to every signal?
    There must be a specific receptor for a cell to respond
  9. What are the different types of receptors and what types of signal molecules does each type interact with?
    • Cell Surface Receptor: large hydrophilic signal molecule binds to cell-surface receptor
    • and
    • Intracelluar Receptor: small hydrophobic signal molecule crosses cell membrane and enters the nucleus or cytoplasm to bind to intracellular receptor
  10. Cell
    Surface Receptors:
    • molecules that are too large/too hydrophilic to cross the plasma membrane
    • therefore binds to the cell surface protein to relay their message across the membrane

    • Signal molecule binds à
    • to the receptor à
    • binding leads to conformational change
  11. Intracellular Receptor:
    Intracelluar Receptor: small molecules/signals which will cross the membrane

    • Once in the cell, intracellular receptor will activate enzymes directly within the cytoplasm or
    • nucleolus – these ligands are permeable to the membrane and will cross
  12. What is Nitric oxide and what is the abbrevivation?
    NO is a hydrophobic molecule, intracellular receptor, readily diffuses adjacent cells
  13. Endothelial cells release Nitric Oxide NO in response to...
    stimulation of nerve ending
  14. NO sigal causes what to occur (hint: relax)
    NO signal casues smooth muscle cells in the vessel wall to relax, allowing blood to run more smoothly
  15. What is stimulated after the nerve cells releases NO?
    NO stimulates relaxation of smooth muscle cells that line the blood vessels = increase blood flow
  16. Total Mechansim of Nitric Oxide
    • Total NO mechanism: Nerve release acetylcholine -->
    • picked up by endothelial cell which converts arginine to NO -->
    • NO diffused into the surrounding smooth
    • muscle cell -->
    • inside the target cell, NO binds to and activates the enzyme guanylyl cyclase, stimulating the formation of GTP to cyclic GMP
  17. Begining with AcH is released by the nerve terminal, name the follow steps relating to Nitric Oxide
    AcH released by nerve cells --> endotheial cells have a receptor --> Release NO --> NO diffuses out of epi cell to bind to guyanlyl cyclase --> controls GTP to cyclic GMP
  18. NO binds to gyanl cylcase -->
    converts GTP to cGMP then reach response of relaxation in smooth muscle cells
  19. Vasodiliation refers to the widening of blood vessels resulting from ...
    • relaxation of smooth muscle cells -- due to NO reaction
    • Viagra prolongs cGMP
  20. NO receptor is (an enzyme) = ??
    NO receptor is (an enzyme) = guanylyl cyclase
  21. NO is hydrophobic
    Intracellular enzyme
  22. Hormone Pathway
    • Hormone
    • -->
    • diffuse into a cell (cytoplasm or nucleus)
    • -->
    • activate receptor (gene
    • regulatory factor)
    • -->
    • gene expression is increased
  23. During an inhibiting state, the steriod will not bind. Once the inhibitor is removed, what will occur and what can we call it?
    • Binding to a steriod = Activation
    • Inhibitor will be removed, and steriod binds to the signal molecule binding domain
  24. What is Hsp90
    Hsp90 will allow inhibitor to be released which will stop all binding
  25. Signal molecules that cannot readily diffuse .......
    • Signal molecules that cannot readily diffuse through
    • membrane bind surface receptors
  26. Ion Channel Linked Receptors : details please
    • the ligand is the binding site
    • signal molecules bind which lead to conformational changes which leads to opening
  27. Receptors are gene regulatory transcription factors
    true
  28. Describe the different types of cell surface receptors
    • Ion channel link receptors: ligand gated
    • channels

    • G-Protein link receptors: could
    • directly or indirectly activate adjacent

    Enzyme-linked receptors
  29. G protein linked receptors (describe)
    • G protein linked receptors are seven pass transmembrane
    • G protein linked receptors transduce the signal through a trimeric GTP-binding protein (G protein) = 3 parts
  30. G protein-link receptor at the Inactive stage
    • Inactive! :
    • 3 subunits (alpha, betta, gamma) are all bound together inactive
  31. G-Protein Receptor: Upon interaction, a signal molecule will bind to the receptor protein....(then what happens)
    • Signal molecule leads to interaction of G-protein (alpha, betta, gamma).
    • Alpha subunit is now active and exchanges GDP for GTP --> seperated
    • Betta-gamma still connected, now released
    • Both subunits can interact with specific target cells
    • The transduction pathway is complete
  32. Alpha subunit itself changes GDP to GTP
    -->
    alpha will activate phospholipase C (with Inositol
    phospholipid) --> ??
    --> IP3 && DAG

    • IP3: diffuse from cytosol,
    • triggers the release of Ca2+ from the ER

    • DAG: remains in the plasma membrane together with Ca2+ where together DAG and Ca2+ will activate
    • PKC (protein kinase C)
  33. What is Ras?
    • Ras is a G-protein which binds and hydrolyzes GDP --> GTP
    • Ras activates the MAP Kinase pathway
  34. how is Ras activated? (enzyme linked receptor)
    • Receptors are usually separated but then will dimerize together -->
    • RTK is activated with it’s adaptor protein-->
    • adaptor of RTK will recruit the Ras-activating-protein that stimulates Ras
    • -->
    • Activated Ras Protein ! -->
    • Ras will now activate the
    • three-kinase pathway = ras-MAP-Kinase pathway --> 321 cell division
  35. Where does the Jak-STAT pathway come from?
    • Enzyme-linked receptor: RTK is activated and will recruit Jak which then activates STAT.
    • STAT gets phosphorlated and will increase gene expression because STAT is a transcription factor - turn genes on
  36. Cell Cycle: series of stages which ...
    • Cell Cycle: series of stages which lead to the cell
    • to divide; prepares the cell to divide
  37. What are the checkpoints and what do they do?
    Checkpoints to make sure all is well before it goes into synthesis and mitosis

    • G1 Checkpoint: (entering S) is the environment
    • favorable

    • G2 Checkpoint: (enter mitosis) is all the
    • DNA replicated or is any DNA damaged?

    • Checkpoint in Mitosis: checks if chromosomes
    • are properly aligned on the metaphase plate
  38. What are the two pathways which come from the activation of the alpha subunit (GDP--> GTP) ?
    signal molecule in receptor--> activate g protein --> alpha subunit -->
    • 1) adenylyl cylase (ATP--> cAMP)
    • 2) phospholipase C --> IP3 & DAG
  39. gprotein/alpha/phospholipase C (inosital phospholipid) --> DAG --> what does it activate?
    DAG plus Ca2+ activates PKC
  40. These small hydrophobic extracellular signal molecules, can diffuse directly across the plasma membrane; activating intracellular proteins, which are usually either transcription regulators or enzymes.
    steriods and Nitric Oxide
  41. G-proteins-coupled receptors and enzyme-coupled receptors respond to extracellular signals by activating one or more intracellular singaling pathways
    true
  42. IP3 opens Ca2+ channels in the membrane of the ER, releasing a free flood of Ca2+ ions into the cytosol
    Ca2+ itself = small intracellular messenger

    What's up with DAG what does it activate
    Ca2+ and DAG activate the PKC
  43. rise in cAMP activates?
    a rise in cyclic AMP activates PKA which
  44. Enzyme-coupled receptors : RTK (receptor tyrosin kinases) which phosphorlates itself ...then this could go two ways: Name
    Ras or Jak/STAT
  45. Ras activates what
    ras activates a three protein MAP-kinase signaling pathway
  46. What controls the G1/S and G2 Checkpoint?
    • controlled by CDK's and cyclin
    • cyclin activate the CDK's
  47. What controls the activity of CDK's?
    • 1) presence of cyclin (high levels present to form CDK cyclin complex)
    • 2) CDK will be phosphorlated which removes the inhibitor
  48. M cyclin: cyclin that acts in G2 to trigger the entry of M-phase
    M cyclin + CDK = M-CDK
  49. Cyclins are activated by mitogens...what are those
    Mitogens are growth factors which stimulate the pathway
  50. (S-CDK) What does the pRb do:
    • S-CDK phosphorylates pRb --> releases E2F
    • E2F binds to specific genes which increase transcription
  51. How does E2F get in the cell and what does it do?
    • S-CDK phosphoralates pRb --> release E2F -->
    • E2F enters nucleus and turns on genes (transcription)
  52. S-CDK What does Cdc6 do?
    • Cdc6 is a part of the origin replication complex
    • S-CDK phosphorylates Cdc6 --> DNA replication and prevention of re-replication
  53. S-CDK can be inhibited if DNA is damaged, what player does that involve?
    • S-CDK will be inhibited if DNA is damaged
    • DNA is damaged --> increase in p53 (transcription factor) --> binds to p21 gene
    • p21 will bind to S-CDK & inactivate it
  54. What regulates the metaphase/anaphase checkpoint or transition of mitosis?
    • APC = Anaphase Promoting Complex
    • - cleavage of cohesions which will lead to ssiter chromatid seperation
    • - triggers destruction of M-cyclin and securin
  55. M-CDK controls the G2 checkpoint and does what?
    • 1) targets phosphorlation of lamins which the nuclear envelope
    • 2) phosphoralats MAPs
  56. If the cell recieves no mitogen (no growth factor), where does it go?
    G0
  57. Compare and contrast necrosis and apoptosis
    • Both necrosis and apoptosis involve cell
    • death.

    Necrosis: death due to damage/external damage like a cut or wound

    Apoptosis: stimulated by the cell/programmed cell death

    - clean, neat, simply chewed up by immune system
  58. What does the protein Bcl-2 family control and what does Bcl-2 (itself) do?
    Bcl-2 family of proteins controls apoptosis BUT Bcl-2 (itself) inhibits apoptosis
  59. What is the pathway for apoptosis?
    (Starts with Bax/Bak)
    • Bax/Bak will lead to cytochromoe C release (mitochondria)
    • --> leads to the activation of caspases
  60. What are caspases ? How do they stimulate apoptosis?
    Caspases are protease which trigger a cascase of other caspases which will chew up the cell; an irreversible process which breaks down the nuclear lamina proteins
  61. What factors stimulate cell divison?
    The cell cycle is regulated by checkpoints, these checkpoints are composes of cyclin-CDK complexes which stimulate the passage
  62. The phosphorylation of CDK will occur in response to ...
    mitogens (growth factor)
  63. Phosphorylation of pRb is by...
    active CDK
  64. When the DNA damage occurs, P53 turns on what....
    • P53 turns on P21 which inhibits CDK
    • --> if there is no ablity to pass through the cell cycle --> G0
  65. Apoptosis is excuted by ....
    caspases

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