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Molecular Foundations of Medicine > Cell Cycle and signaling > Flashcards

Cell Cycle and signaling Flashcards

1
Q

Intracellular hormones

A
  • lipid/fat soluble -> can cross plasma membrane
  • receptors are in cytoplasm or nucleus
  • Not soluble in plasma -> circulate bound to a protein
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2
Q

examples of lipid soluble hormones

A
  • progesterone
  • estrogen
  • testosterone
  • cortisol
  • aldosterone
  • thyroid hormone
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3
Q

circulatory protein for estrogen/testosterone

A

sex binding globulin (SBG)

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4
Q

circulatory protein for thyroid hormone

A

thyroid binding globulin (TBG)

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5
Q

circulatory protein for cortisol, aldosterone, and progesterone

A

corticosteriod binding globulin (CBG)

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6
Q

extracellular hormones

A
  • Not lipid soluble
  • bind to surface receptors
  • can either directly drive cellular changes, or use 2nd messenger system
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7
Q

extracellular hormone receptors that don’t use 2nd messenger

A
  • tyrosine kinase

* JAK/STAT

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8
Q

important 2nd messengers

A
  • cAMP
  • cGMP
  • IP3
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9
Q

receptor tyrosine kinase

A

EX: insulin binds -> RTK auto-phosphorylates -> gene transcription
*NO 2nd messenger
•many growth factors also use RTKs: IGF-1 (insulin-like), FGF (fibroblast), PDGF (platelet-derived), EGF(epidermal)

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10
Q

JAK/STAT

A
  • JAK = janus kinase -> tyrosine kinase enzyme
  • STAT = signal transducer and activator of transcription
  • when the receptor is bound, JAK is activated to phosphorylate STAT which can then activate transcription
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11
Q

hormones that use JAK/STAT

A
  • many cytokines (IFN-γ, IL-2, IL-6)
  • erythropoietin
  • G-CSF (granulocyte-colony stimulating factor)
  • thrombopoietin
  • prolactin
  • growth hormone
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12
Q

JAK2 mutation

A

•JAK2 = gene for cytoplasmic tyrosine kinase
•mutation -> increased tyrosine phosphorylation -> hypersensitivity to cytokines -> more growth/longer survival
∴associated with myeloproliferative disorders

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13
Q

adenylyl cyclase

A

converts ATP to cAMP

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14
Q

receptors that use cAMP as second messenger

A

G-protein linked receptors

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15
Q

Hormones that use cAMP as 2nd messenger

A
  • hypothalamus -> CRH, GHRH
  • ant. pituitary -> FSH, LH, ACTH, TSH
  • parathyroid hormone (PTH)
  • glucagon
  • ADH
  • Histamine (H2-receptor -> GI)
  • hCG
  • MSH (melanocyte stim)
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16
Q

guanylate cyclase

A

converts GTP to cGMP

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17
Q

substances that use cGMP as 2nd messenger

A

•BNP/ANP
•Nitric oxide
(all are vasodilators)

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18
Q

phospholipase C

A

converts PIP2 to IP3

phosphatidyl inositol bisphosphate; inositol triphosphate

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19
Q

receptors that use IP3 as second messenger

A

G-protein linke receptors

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20
Q

Hormones that use IP3 as second messenger

A
  • hypothalamus: GnRH, TRH
  • post. pituitary: oxytocin and ADH (only V1 receptor -> vasoconstriction)
  • Histamine (H1 receptor -> skin lungs)
  • angiotensin II
  • gastrin
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21
Q

Cell cycle events

A

G1 -> S -> G2 -> M -> G1 or G0 (quiescent)

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22
Q

Interphase

A

G1, S, and G2

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23
Q

G1 phase

A
  • synthesis of proteins and organelles

* length varies

24
Q

mitogens

A
  • extracellular signaling molecules
  • stimulate cell division
  • function via cyclin dependent kinases (CDKs)
25
Q

Growth factor

A

stimulates growth in size

26
Q

S phase

A
  • synthesis of DNA

* chromosomes -> 2 sister chromatids

27
Q

G2 phase

A

•growth in preparation for mitosis

28
Q

G0 phase

A
  • may occur in absence of mitogen stimulation
  • non-dividing state
  • most cells in our body are in G0, some permanently
29
Q

Neurons and skeletal muscle cells are

in terms of cell cycle

A
  • terminally differentiated

* permanent G0 state

30
Q

Liver cells are

in terms of cell cycle

A

often in G0, but can divide if stimulated

31
Q

fibroblasts and lymphocytes are

(in terms of cell cycle

A

enter/exit G0 many times in lifespan

32
Q

labile cells

A
  • bone marrow, GI epithelial cells, hair follicles
  • rapidly divide -> rarely/never enter G0
  • most effect by chemotherapy
33
Q

mitosis

A
  • shortest/most rapid part of cell cycle

* Prophase -> prometaphase -> metaphase -> anaphase -> telophase

34
Q

prophase

A
  • chromosomes condense

* spindle fibers form (mitotic spindle)

35
Q

prometaphase

A

chromosomes organize on mitotic spindle

36
Q

metaphase

A

chromosomes line up on metaphase plate

37
Q

anaphase

A

chromosomes separate

38
Q

telophase

A
  • spindle breaks down

* cell divides

39
Q

G1-S checkpoint

A
  • prior to S phase entry
  • where the cell commits to divide into 2 daughter cells
  • mitogens activate CDK -> S phase
40
Q

G2-M checkpoint

A

prior to mitosis

41
Q

M phase checkpoint

A

prior to anaphase/cytokinesis

42
Q

cyclin dependent kinases (CDKs)

A
  • central components of cell cycle control

* always present, but inactive until cyclins activate it

43
Q

cyclins

A

regulatory proteins that activate CDKs

44
Q

cyclin-CDK complexes

A
  • phosphorylate regulatory proteins

* allow progression through cell cycle

45
Q

how does mitogen activation of CDK occur

A

bind cell surface receptor -> activate intracellular pathways -> increase G1 cyclin levels -> increase CDK activity

46
Q

E2F proteins

A
  • activated by cyclin-CDK complexes at G1-S checkpoint

* bind to DNA promoter regions -> activate genes necessary for entry to S phase

47
Q

inhibition of E2F

A

•normally inhibited by binding retinoblasoma (rb) proteins
•phosphorylation of rb by G1-S-CDK releases inhibition
∴rb regulates cell growth (“tumor suppressor”)

48
Q

ATM pathway

A
  • =ataxia telangiectasia mutated
  • activated by double stranded DNA breaks
  • leads to phosphorylation of proteins -> cell arrest at G1-S checkpoint
49
Q

ATR pathway

A
  • =ATR and RAD3 related
  • activated by single stranded DNA breaks
  • leads to phosphorylation of proteins ->cell arrest at G1-S checkpoint
50
Q

P53 protein

A
  • major target of phosphorylation in ATM/ATR systems
  • becomes phosphorylated with DNA damage ->induces transcription of P21 protein
  • tumor suppressor
51
Q

P21 protein

A
  • binds to CDKs and inhibits their activity -> blocks progression through cell cycle
  • tumor suppressor
52
Q

retinoblastoma

A
  • rare childhood eye malignancy
  • mutations in RB1 gene -> codes for rb protein
  • abnormal rb -> unregulated cell growth (via E2F)
53
Q

Li-Fraumeni syndrome

A
  • multiple malignancies at early age

* caused by mutations in tumor suppressor gene TP53 -> cell cycle not arrested to allow for DNA repair

54
Q

Ras/Raf system

A
  • many growth factors bind RTKs that activate Ras/raf system
  • Ras uses GTP->GDP and binds to Raf (MAPKKK) -> phosphorylates MEK (MAPKK) -> phosphorylates ERK (MAPK) -> phosphorylates transcription factors (ie cyclin D and E)
  • MAPK = mitogen activated protein kinase
55
Q

cyclin D

A
  • mitogen sensing

* expressed throughout cell cycle

56
Q

Rationale for using radiation therapy for some cancers

A

Cleavage of DNA double strands crucial for S phase and rapidly growing cells

Molecular Foundations of Medicine (21 decks)

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