BICD 110 Lecture Notes - Lecture 16: Hemolytic Disease Of The Newborn, Harold E. Varmus, Myc
28 Jun 2018
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BICD110 Lecture 16 Notes 5/29/18
- Cell in a multicellular organism comes out of the G0 phase and goes into S phase using
growth factors like EGF and PDGF
oCyclin/CDK heterodimers rule the cell cycle
CDK1/cyclin B (mitotic kinase) regulates mitosis
CDK2/cyclin E (G1/S kinase) regulates the transition from the G1 to S phase
Complex consists of the regulatory cyclin (carpenter) + catalytic cyclin-dependent
kinase (CDK) (hammer)
- Function of growth factors
oMost bind a cell surface receptor. The EGF receptor is a
tyrosine kinase
oWhen the EGF receptors bind EGF, they dimerize and
their kinases turn on and phosphorylate the other dimer
partner. This activates the kinases and causes them to
phosphorylate downstream proteins
oThe signal cascades, in which the signal enters the
nucleus for transcription
oDNA replication (S phase) -> G2 -> M -> CK -> 2 cells
oThe PDGF receptor is also a tyrosine kinase
- What goes wrong in cancer? Normal vs. Cancer cells
o1) Normal cells need GFs to divide (EGF and PDGF), but cancer cells often don’t
o2) Normal cells need to adhere to a substratum to divide. Cancer cells don’t
o3) Normal cells possess well-organized actin cytoskeleton like stress fibers; cancer cells
don’t
o4) Normal cells show density-dependent inhibition of growth. They recognize one
another; form a monolayer, then stop dividing. Cancer cells growth on top of each
other; they don’t exhibit density-dependent inhibition
o5) Normal cells divide a set number of times (~50), then stop (senescence, undergo
apoptosis), because normal cells have low telomerase and can no longer copy ends of
chromosomes. Cancer cells are immortal (just keep on dividing) because they have LOTS
of telomerase
Telomerase is very low in normal cells; good but age causes problems
Shortening each division, then loss of telomeres leads to cell death
Telomerase is high in cancer cells, so they have longer telomeres
No senescence, no cell death
Telomerase is high in normal stem cells; keeps telomeres long so stem cell
population can keep dividing and is long-lived
Elizabeth Blackburn (UCSD, Salk) and Carol Greider (UCSB, UCB, born in SD, won
2009 Nobel Prize for telomerase with Jack Szsotak)
o6) Normal cells undergo apoptosis when their DNA is damaged (programmed cell
death). Cancer cells don’t. They keep dividing even with DNA damage
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Cell in a multicellular organism comes out of the g0 phase and goes into s phase using growth factors like egf and pdgf: cyclin/cdk heterodimers rule the cell cycle. Cdk2/cyclin e (g1/s kinase) regulates the transition from the g1 to s phase. Complex consists of the regulatory cyclin (carpenter) + catalytic cyclin-dependent kinase (cdk) (hammer) Function of growth factors: most bind a cell surface receptor. The egf receptor is a tyrosine kinase: when the egf receptors bind egf, they dimerize and their kinases turn on and phosphorylate the other dimer partner. Normal vs. cancer cells: 1) normal cells need gfs to divide (egf and pdgf), but cancer cells often don"t, 2) normal cells need to adhere to a substratum to divide. Cancer cells don"t: 3) normal cells possess well-organized actin cytoskeleton like stress fibers; cancer cells don"t, 4) normal cells show density-dependent inhibition of growth. They recognize one another; form a monolayer, then stop dividing.
