CAS BI 206 Chapter Notes - Chapter 17: Ras Subfamily, Nuclear Membrane, Dna Replication

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Chapter 17
โ—Cell division is initiated via two types of signals
โ—‹Extracellular signals๎€ local/long distance signalling molecules
โ—‹Cell-bound signals๎€ fingerprints for the bodyโ€™s cells
โ—Cell division signaling system is composed of ๎€growth factors๎€, ๎€receptors๎€, ๎€signal transducers๎€, and
transcription factors
โ—RAS protein๎€ in off form: RAS-GDP; in on form: RAS-GTP; binding of growth factor to receptor
turns RAS on โ‡จ activates protein kinases in ๎€MAP kinase cascade๎€ โ‡จ transcription factor
Cancer
โ—Cancer is result of accumulation of mutations during somatic cell proliferation
โ—Properties of cancer cells
โ—‹Autocrine stimulation๎€ create their own stimulatory signaling molecules โ‡จ stimulate own
growth
โ—‹Loss of contact inhibition๎€ cells normally stop division when in contact with others โ‡จ
cancers don't
โ—‹Loss of cell death๎€ cancer cells are resistant to programmed cell death via apoptosis
โ—‹Loss of gap junctions๎€ cancer cells donโ€™t have junctions that promote transfer between
cells
โ—Cancer emerges as result of environment/mutations over time; are not (usually) inherited
โ—Predisposition to cancer can be inherited
โ—‹RB gene๎€ retinoblastoma; half of people w retinoblastoma inherit a mutation in RB gene
โ‡จ one mutant copy โ‡จ mutation in one remaining gene โ‡จ cancer (normal ppl need
mutation in both)
โ—Oncogenes๎€ dominant mutations that increase cell proliferation
โ—‹Increased growth =/= cancer โ‡จ increased growth + other effects = cancer
โ—‹More cells = more chance of mutation = increased chance of cancer
โ—Tumor-suppressor genes๎€ recessive mutations increase cell proliferation
โ—‹Common ones: ๎€RB๎€, ๎€p53๎€, ๎€p16
โ—‹Single copy (one mutant) usually is enough protein to regulate division โ‡จ 2 mutations
needed
โ—‹RB gene๎€ recessive inheritance of gene but dominant retinoblastoma trait โ‡จ strong
likelihood that one of the heterozygous RB+- cells will mutate โ‡จ no RB gene
Cell Division
โ—Cell division๎€ normally consists of ๎€G1๎€ growth gap after mitosis; ๎€S๎€ DNA replication; ๎€G2๎€ gap
between DNA replication and mitosis; division preparation; ๎€M๎€ mitosis
โ—‹Mutations that interfere with cell cycle are lethal bc cell cannot properly grow
โ—Cyclin-dependent kinases (CDK)๎€ family of kinases that regulation transitions between phases
through phosphorylations that (in)activate target proteins
โ—‹Cyclin portion of CFK specifies target proteins for that CDK
โ—‹CDK cycle is managed via
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Document Summary

Cell division is initiated via two types of signals. Cell-bound signals fingerprints for the body"s cells transcription factors. Cell division signaling system is composed of growth factors , receptors , signal transducers , and. Ras protein in off form: ras-gdp; in on form: ras-gtp; binding of growth factor to receptor turns ras on activates protein kinases in map kinase cascade transcription factor. Cancer is result of accumulation of mutations during somatic cell proliferation. Autocrine stimulation create their own stimulatory signaling molecules stimulate own. Loss of contact inhibition cells normally stop division when in contact with others . Loss of cell death cancer cells are resistant to programmed cell death via apoptosis. Loss of gap junctions cancer cells don"t have junctions that promote transfer between cancers don"t cells. Cancer emerges as result of environment/mutations over time; are not (usually) inherited. Rb gene retinoblastoma; half of people w retinoblastoma inherit a mutation in rb gene.

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