Shuia.txt

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emm64
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114241
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Shuia.txt
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2011-11-03 11:42:06
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Foundations Shuai
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Foundations Shuai
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  1. Ubiquitin
    • Covalent conjugation attached to lysine residues of substrates.
    • E1(activation, needs ATP), E2(conjugation), E3(Ligase, high specificity based on UB signal)
    • targeted by multisubunit ATP-dependent protease known as the 26S proteasome for degradation
  2. APC: anaphase-promoting complex
    • aka E3 Ligase of ubiquitin, matches to mitotic cyclin destruction box
    • Late ANaphase, APC polyubiquitinates mitotic cyclins
    • cyclin down, MPF(CDK and cyclin) activity down -> Telophase
  3. Cdh1
    • regulator of APC
    • Inactivated when phosphorylated by G1 cyclin CDK -> mitotic cyclin increases->promote mitosis entry
  4. Cdc14
    • removes the phosphate from Cdh1 late in anaphase to activate APC->polyubiquitation of cyclin
    • Lack CDC->no decrease in Cyclin-> long cells
    • Overactive CDC-> cyclin cycle too short-> premature telophase
  5. G2 events
    Spindle Pole Body Duplication
  6. Cdk Activity Regulation
    • Phosphorylated in order by Wee1 CAK
    • Cdc25 phosphotase of P of Wee1 to activate CDk
    • No CDC 25-> No MPF activity-> increased G2 elongated cells
    • Too much Wee1 -> No MPF activity -> increased G2 elongated cells
    • No Wee1-> No inhibition of MPF-> too much mitosis-> premature small cells
    • Too much CDC25-> Too much MPF -> too much mitosis-> premature small cells
  7. Cyclin-kinase inhibitors (CKIs)
    • two classes:
    • CIP (Cdk inhibitory protein)
    • INK4 (inhibitors of kinase 4)
    • CIP: p21, p27, and p57.
    • CIP inhibits all cyclin-Cdk complexes.
    • INK4 inhibits only Cdk4/6-cyclin D complexes.
    • Binding of CKIs to cyclin-Cdk complexes leads to cell cycle arrest.
  8. MPF(CDK) activity
    phosphorylate nuclear lamins to breakdown nuclear envelope
  9. Cdc20
    • APC specificity factor that ubiquinates Securin
    • Securin is the muzzle on Separase(pacman) that separtates sister chromatids by cutting Scc1
  10. Different Cyclins
    • different cyclins control different cell cycle stages through restriction points
    • Cyclin D->restriction point of G1
  11. E2F transcription factors
    • stimulate transcription required for DNA replication, deoxyribonucleotide synthesis as well as Cdk2, cyclin A and cyclin E.
    • E2F inhibited by binding of hypophosphorylated Rb protein, a product of tumor-suppressor gene RB.
    • G1->S transition requires activation of E2Fs
  12. Cancer Changes
    • Sustained Angiogenesis
    • Tissue Invasion and metastasis
    • Limitless replication Potential
    • Self-sufficent growth signals
    • Insensitvity to anti-growth signals
    • Evasion of Apotosis
  13. Tumor cell properties
    • Immortilization
    • Transformation
    • Metastasis
  14. Oncogenes
    whose products have the ability to transform eukaryotic cells so that they grow in a manner analogous to tumor cells. Oncogenes alone are not sufficient to cause cancer. Inactivation of tumor suppressors is a major event leading to the development of cancer
  15. Proto-oncogenes
    normal cellular genes known to be progenitors of oncogens
  16. Tumor-suppressor genes
    encode proteins that inhibit the progression of tumors.
  17. Amplification
    localized reduplication (gene amplification) of a DNA segment, leading to overexpression of the encoded proteins.
  18. BCL
    wants to fuck with apoptotic proper sequence by binding to Bax, but Bad prevents that. Bax and Bad are pro-apoptotic.
  19. Oral cancer
    • Over-expression TGF-alpha, stimulates cell proliferation.
    • EGF receptor gene amplification
    • Ras mutations
    • transcription factor c-Myc which helps regulate cell proliferation is frequently overexpressed
    • Anti-apoptosis proteins Bcl-2 overexpression
    • Cell cycle control proteins Cyclin D is amplified
    • Inactivation of p53(CDK Inhibitor)
  20. p53
    • Regulated by post-translational modifications: phosporylation acetylation, ubiquitination
    • Regulated by a number of protein factors. MDM2 is a ubiquitin ligase which negatively regulates p53 activity. MDM2 targets p53 for degradation and can repress the transcriptional activity of p53. MDM2 is induced by 53---- a negative feed back control.
    • p53 mutation is dominant.
    • p53 regulates cell cycle (p21) and apoptosis(Bax)
    • Cigarette smoking--> benzopyrene-->metabolic activation-->
    • T transversion mutation-->aa 175, 248, 273 mutations-->60% lung cancer containing p53 mutations.
  21. Src
    • proto-oncogene encoding a tyrosine kinase
    • v-src lacks the C-terminal inhibitory phosphorylation site (tyrosine-527), and is therefore constitutively active as opposed to normal src (c-src)
  22. c-myc
    proto-oncogene whose expression can be enhanced and promoted by viral genes

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