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Comprehensive Review > Molecular Review (White) > Flashcards

Molecular Review (White) Flashcards

1
Q

endocrine signaling

A
  • long distance signaling
  • long lasting, freely diffusible signals
  • moves through bloodstream
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2
Q

paracrine signaling

A
  • acts locally

- short lived, affects nearby cells

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3
Q

synaptic signaling

A
  • acts locally

- short lived, NEUROTRANSMITTERS

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4
Q

autocrine signaling

A
  • cells respond to signals that they themselves release or release to cells of the same type
  • growth factors –> cells grow, divide, mature
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5
Q

direct cell signaling

A
  • immune cells

- Ag presentation to T cells

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6
Q

G protein coupled receptors

A
  • extracellular domain: binds ligand
  • transmembrane domain: anchors receptor
  • cytoplasmic domain: associated with G protein

associates with heterotrimeric G proteins –> alpha subunit regulate target enzymes (activated G protein)

  • alpha subunit binds GTP –> activates adenylyl cyclase
  • alpha subunit binds GDP –> binds to beta subunit (inactive)
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7
Q

Cholera and G protein

A
  • cholera toxin keeps G-alpha in GTP active form indefinitely
  • pump Cl/water out of cells in intestine and causes severe diarrhea
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8
Q

cAMP

A
  • generated by adenylyl cyclase –> interacts with target protein to cause biological response
  • activates PKA (2 cAMP molecules bind to regulatory subunits of PKA which releases 2 catalytic subunits)
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9
Q

Receptor Tyrosine Kinases (RTKs)

A
  • enzyme-linked receptors (enzymatic domain in cytoplasm) –> transmit signal through tyrosine kinase domain
  • used for response to growth factors
  • adds phosphate to tyrosine on proteins
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10
Q

Receptor Tyrosine Kinase activation

A
  • ligand binding causes dimerization (autophosphorylation occurs)
  • acts as scaffold to recruit other proteins to plasma membrane (Grb2 –> SH2 binds)
  • SH3 domain of Grb2 binds SOS, which binds Ras (SOS is GEF that adds GTP to Ras)
  • Ras binds Raf –> activates MAP kinase pathway (phosphorylates and makes changes in protein activity and gene expression)
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11
Q

What was the first discovered human oncogene?

A

Ras

  • plays crucial role in cell division and a frequent mutation in cancer
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12
Q

JAK-STAT receptors

A
  • ligand binds to receptors (dimerization) then bind JAK
  • JAK phosphorylates each other and the receptor
  • STATS bind and are phosphorylated by JAK
  • STATS dimerize and enter nucleus –> bind DNA and cause transcription of target genes
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13
Q

Serine-threonine receptor and Smad

A
  • ligand binds type II receptor, which phosphorylates second receptor (type I)
  • Type I phosphorylates R-Smad, which associates with Co-Smad
  • moves into nucleus to impact transcription of target genes
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14
Q

helix-turn-helix

A
  • simplest DNA-binding motif
  • 2 alpha helices connected by short chain of AAs
  • longer helix portion = recognition module (DNA binding module)
  • bind DNA as dimers
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15
Q

zinc finger domain

A
  • DNA binding motif with Zn atom

- binds to major groove of DNA

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16
Q

Leucine zipper motif

A
  • two alpha helical DNA binding domain
  • dimerization through leucine zipper region
  • grabs DNA like clothespin
  • hydrophobic AA side chain interactions at every 7 AA down one side of alpha helix
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17
Q

helix-loop-helix

A
  • short alpha chain connected by loop to second longer alpha chain
  • can occur as hetero or homodimer
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18
Q

RNA stability regulation

A
  1. remove 5’ cap –> mRNA degraded from 5’ end

2. mRNA degraded from 3’ end through poly-A tail

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19
Q

Checkpoints of the Cell Cycle (3)

A

Checkpoint 1: Start –> cell commits to cell cycle entry and chromosome duplication

Checkpoint 2: G2/M –> move into chromosome alignment on spindle in metaphase

Checkpoint 3: metaphase-to-anaphase transition - trigger sister chromatid separation and cytokinesis

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20
Q

Cdks

A
  • heart of cell cycle control system
  • dependent on cyclins (must be bound to cyclin to have protein kinase activity)
  • activities rise and fall during cell cycle
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21
Q

CAK

A
  • causes phosphorylation at T-loop of Cdk (normally blocks active site) –> fully activates enzyme
  • cyclin binding causes T-loop to move out of active site
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22
Q

condensins

A
  • help reorganize sister chromatids to be pulled apart during anaphase with NO breakage
  • chromosomes condensation and resolution
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23
Q

M-Cdk

A
  • activates APC/C to complete mitosis
  • ubiquitinates and causes degradation securin and allows separase to activate
  • separase cleaves cohesins, causing metaphase to enter anaphase (pull apart sister chromatids)
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24
Q

Two major classes of caspaces

A
  • synthesized as inactive precursor (procaspases)
  • initiator caspases and executioner caspases
  • executioner destroys actual targets (apoptosis)
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25
Q

Intrinsic Apoptosis

A

cytochrome c released from mitochondria binds to Apaf1 –> assembles into apoptosome and recruits caspase-9

caspase-9 cleaves and activates executioner procaspases (APOPTOSIS)

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26
Q

BH123

A

form aggregation in mitochondrial outer membrane, releasing cytochrome C

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27
Q

Bcl2

A

prevents aggregation of BH123 (inhibits apoptosis)

28
Q

BH3

A

apoptotic stimulus that inactivates Bcl2 proteins

  • allows BH123 to assemble
29
Q

IAPs

A

bind to caspases and prevent their activity

30
Q

anti-IAPs

A
  • released from mitochondria and bind to IAPs

- prevent IAP association with caspases, allowing for normal executioner caspase activity

31
Q

Overactivity vs Underactivity mutations

A

Overactivity - GAIN OF FUNCTION (oncogenes) –> single mutation event, activation of gene causing proliferation (dominant)

Underactivity - LOSS OF FUNCTION (tumor suppressor genes) –> one mutation, no effect; two mutations, cause problem (recessive): involve genes that inhibit growth

32
Q

Hereditary Retinoblastoma

A
  • loss of function/deletion of one copy of Rb in every cell (defect inherited)
  • somatic event occurs that eliminates the good copy = tumor formation (loss of heterozygosity)
33
Q

Sporadic Retinoblastoma

A
  • non-hereditary

- first Rb gene obtains mutation, increasing the likelihood that second gene mutates

34
Q

Polyp

A
  • precursor of colorectal cancer
  • slow progression (10 years)
  • cut off polyp = CURE
35
Q

Colorectal Cancer mutations (3)

A

> 80% –> loss of Apc (tumor suppressor gene)

40% –> point mutation in K-Ras

60% –> loss of p53

36
Q

Actin Filaments

A
  • determine shape of cell’s surface and are necessary for whole-cell locomotion, secretion, endocytosis
37
Q

Microtubules

A
  • forms tube-like structure
  • determine the positions of membrane-enclosed organelles
  • direct intracellular transport
38
Q

Intermediate Filaments

A
  • provides mechanical strength, strong filament

- resists mechanical stress, allow formation of hair/fingernails

39
Q

Actin filament assembly

A
  • monomer contains ATP/ADP binding
  • two protofilaments that twist around each other (right handed helix)
  • held together by lateral contacts (arranged head-to-tail
  • flexible, easily bent
40
Q

Tubulin assembly

A
  • formation of microtubules
  • end-to-end and side-to-side protein contacts
  • heterodimer of a/B tubulins (binding sites for GTP)

(+) end –> fast growing/shrinking end
(-) end –> slow growing/shrinking end

41
Q

Hereditary Spherocytosis

A
  • RBCs spherical, not bi-concave (get shape from cytoskeleton, defective SPECTRIN –> durability/stability)
  • fragile RBCs burst = hemolytic anemia
42
Q

Listeria

A
  • pathogenic bacteria that invade intestinal cells
  • causes food poisoning especially if immunologically deficient or immunocompromised
  • smashes through organelles (leaves actin track aka ‘comet trails’)
43
Q

Listeria and ARP (Arp 2/3)

A
  • Arp complex is responsible for generating the actin trails that Listeria uses to move
  • actin branch filaments pushes the bacteria
44
Q

Duchenne Muscular Dystrophy

A
  • most common fatal neuromuscular disorder in boys
  • severe, progressive muscle degeneration
  • patients in wheelchairs by 12 years of age
  • no medical treatment, just maintain patients general health and improve quality of life
45
Q

Duchenne Muscular Dystrophy genetics

A
  • X linked recessive

- caused by dystrophin gene mutations; present at birth but does NOT show symptoms until about 3 years of age

46
Q

What is the main function of the dystrophin protein?

A

to provide structural stability to the muscle cell membrane during contraction and relaxation

  • 4 functional domains
47
Q

4 functions domains of dystrophin

A
  1. N-terminus (actin binding domain)
  2. Long spectrin-like repeat domain
  3. Cysteine rich domain
  4. C-terminus domain
48
Q

Dystrophic myopathy

A

progressive muscle degeneration w/loss of functional muscle tissue over time with resulting weakness

49
Q

DMD Clinical Presentation

A

necrosis of muscle fibers occurs with replacement of fat or connective tissue

  • leads to pseudohypertrophy: replacement of muscle w/adipose tissue and fibrous CT (enlarged calves)
50
Q

Lordosis vs Kyphosis

A

Lordosis: excessive inward curvature

Kyphosis: upward back curvature outward

51
Q

Gower Maneuver

A
  • boys with DMD rising from floor

- first get on hands and knees, then elevate posterior, then ‘walk’ their hands up the legs to raise upper body

52
Q

Becker Muscular Dystrophy

A
  • milder than Duchenne (similar symptoms but milder)
  • increased workload on left ventricle = left ventricular enlargement (severity results in heart failure and death)
  • some dystrophin protein of abnormal quantity and size (Duchenne = NO dystrophin)
53
Q

Mitochondrial Myopathies w/Ragged Red Fibers

A
  • degeneration of muscle fibers caused by accumulation of abnormal mitochondria
  • abnormal mitochondrial aggregates for red sarcolemmal blotches (Ragged Red Fibers)
54
Q

heteroplasmy

A

mixture of normal and mutant mitochondria in one cell

  • threshold effect of mutant mitochondria are required for disease manifestation
55
Q

MERRF

A
  • myoclonus epilepsy
  • INVOLUNTARY JERKING
  • ataxia, myclonic epilepsy, ragged red fibers
  • 90% caused by 2 mutations of tRNA(Lys)
56
Q

MERFF Mutations (2)

A

85% –> due to A to G mutation

5% –> due to G to C mutation

57
Q

MELAS

A
  • Mitochondrial Encephalopathy, Lactic Acidosis with Stroke-like episodes
  • onset = 2-10 years
  • BLINDNESS, Ragged Red Fibers, vomiting, anorexia, headaches, seizures
  • mutation in tRNA(Leu) –> A3243G
58
Q

Kearns-Sayre Syndrome

A
  • retinosis pigmentosa (degenerative eye disease leading to blindness
  • onset before age 20
  • at least one: cardiac conduction abnormality, cerebellar ataxia, cerebral spinal protein level above 100 mg/dL
  • 85% of KSS due to mtDNA rearrangements
59
Q

Chronic Progressive External Ophthalmoplegia (CPEO)

A
  • mild to moderate mitochondrial myopathy (ragged red fibers observed in skeletal muscle) –> mtDNA rearrangements
  • PTOSIS (drooping of eyelid)
60
Q

Leber Hereditary Optic Neuropathy (LHON)

A
  • mitochondrial mutation ONLY affects optic nerve
  • acute or subacute, bilateral, central vision loss
  • degeneration of retinal ganglion cell layer and optic nerve
  • initially affects one eye but eventually both eyes affected at the same time (Maternal inheritance)
61
Q

Hemoglobin Structure

A
  • multi-subunit protein (tetramer) –> 2 alpha/beta chains

- heme: one per subunit, has iron atom

62
Q

4 types of hemoglobin chains

A

alpha, beta, delta, gamma

63
Q

Hemoglobin forms

A

HbA –> 2 alpha and 2 beta chains (adult form)

HbA2 –> 2 alpha and 2 delta (3%)

HbF –> 2 alpha and 2 gamma (fetal form) (0.5%)

64
Q

Sickle Cell Anemia and HbF

A
  • sickle shaped RBCs that impede circulation = hemolytic anemia
  • HbS–> substitution of valine for glutamic acid at AA #6
  • use hydroxyurea to induce HbF
65
Q

Modular HbF

A
  • fetus needs Hb that has higher affinity for oxygen than mother’s Hb
  • HbF does not bind well to 2,3-BPG = has a HIGHER affinity for oxygen

Comprehensive Review (7 decks)

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