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IBSS 501 > Module 1 > Flashcards

Module 1 Flashcards

1
Q

Types of Multipotent Cells

A

Hematopoietic, Mesenchymal, Skin, Neural, and Epithelial

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2
Q

Stem cell commitment

A

is a stepwise process, transcription factors turn certain developmental pathways on and shut others off (this determines what cell type it will become)

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3
Q

Asymmetric cell division

A

maintains stem cell populations by creating two different daughter cells from mitosis. one daughter cell is a stem cell while the other has the ability to differentiate (due to cell polarity during cell division this daughter cell does not have any proteins that help keep the cell in stem cell form)

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4
Q

Induced pluripotent stem cells

A

aka cellular reprogramming, this is done by the overexpression of stem cell maintenance proteins in somatic (unipotent) cells

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5
Q

Where are stem cells found in the human body?

A

Umbilical cord blood, dental pulp of mandibular third molars, deciduous teeth that have been shed, and periodontal ligament cells

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6
Q

Stem cell niche

A

saves stem cells from depletion and protects the human from overproduction of stem cells. ECM interactions are known to play an important role in maintaining the niche

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7
Q

Glycoaminoglycans (GAG) structure

A

Repeating dissacharide chains of acidic sugar-acetylated sugar
Negative surface charge
covalently attach to proteins to form proteoglycans
proteoglycan aggregates –> fir tree appearance

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8
Q

Collagen Synthesis

A
  1. translation into RER
  2. vitamin C dependent hydroxylation of pro and lys residues
  3. some hydroxylysine residues are glycosylated
  4. triple helix formation
  5. secretion into ECM and cleavage
  6. formation of mature collagen
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9
Q

Elastin

A

enables skin to stretch without tearing (lungs, arteries etc)
contains little hydroxyproline and no hydroxylysine
interacts with fibrillin in ECM
form desmosine cross links

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10
Q

Fibrous Proteins and disease

A

Scurvy - vitamin C deficiency
Osteogenesis Imperfecta - abnormal collagen (type 2 lethal) or decreased collagen (type 1)
Ehlers-Danlos Syndrome - defects in collagen causing stretchy skin
Marfan Syndrome - defect of fibrillin-1 tall and thin long fingers
a1-antitrypsin deficiency - reduced ability to inhibit elastase from neutrophils in lungs which causes breakdown of lung tissue

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11
Q

Adhesive proteins

A

join ECM components to eachother and cells to the ECM
fibronectin - connective tissues
laminin - epithelial tissues

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12
Q

Cell adhesion molecules

A

Cadherins
Selectins
Immunglobulin Superfamily
Integrins

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13
Q

Cadherins

A

Ca2+ mediated cell-cell adhesion
1 cadherin binds to another in the ECM by joining actin of the cytoskeletons
major role in holding cells together and tissue integrity

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14
Q

Selectins

A

transiet cell-surface binding
connects cells by binding protein on surface of one cell to carbohydrate on the surface of another
important in the bloodstream with WBC

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15
Q

Immunoglobulin Superfamily

A

cell-cell adhesion with transient expression

important during development and regeneration

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16
Q

Integrins

A

Both cell-cell AND cell-ECM adhesion
integrins bind to fibronectin and laminin in the ECM (depends on tissue type)
multiple weak adhesions due to low binding affinity

17
Q

Hetero vs euchromatin

A 
heterochromatin = more tightly packed and less transcription
euchromatin = less tightly packed and more genes are located within this region
18
Q

Ribosomes

A

40% protein and 60% rRNA

19
Q

Treacher Collins Syndrome

A

genetic disorder affecting ribsome biogenesis

defective treacle gene causing improper trxn of rRNA for 28S subunit

20
Q

Rapid growth (RER vs SER)

A

during rapid growth there is a lower concentration of RER which means less proteins are being secreted outside of the cell to meet the metabolic demands inside the cell

21
Q

Cystic Fibrosis

A

mutations in the CFTR gene that distrupt normal protein conformation and traps proteins in the ER (which normal deals with the unfolded protein response to correctly fold proteins)

22
Q

Peroxisomal disorders

A

X-linked adrenoleukodystrophy

Zellweger syndrome

23
Q

Lipids in each leaflet

A

Outer - SM and PC

Inner - PI, PE, PS

24
Q

FRAP

A

shows that proteins can redistribute throughout the lipid bilayer

25
Q

Lipid rafts

A

cholesterol enriched microdomains in the plasma membrane

functions include cholesterol transport, endocytosis, signal transduction

26
Q

spectrin

A

actin binding protein that provides stability, strength, support for the plasma membrane
spectrin forms dimers and then tetramers with itself

27
Q

Actin

A

regulation of physical state of cytosol (gel/sol state)
cell movement
contractile rings during cell division

G-actin monomers hydrolyze ATP to polyermize into F-actin. eventually reaches a steady state where rate of addn to the PLUS end=rate of sub to the MINUS end

28
Q

Actin binding proteins

A
  1. regulators of gel/sol state
  2. spectrin (association requires ATP & important in RBC)
  3. dystrophin (in skeletal muscle cells)
29
Q

intermediate filaments

A

do not disassemble and assemble rapidly like actin and microtubules
stable & intact structures in the cell
fibrous and provide structural support

30
Q

microtubules

A

motility, chromosomal movements, organelle and vesicle transport
protofilaments form cylindrical structure and GTP bound heterdimers (composed of alpha and beta tubulin) add to the plus end, this is called the GTP cap
Once the GTP cap is gone, the microtubule cannot grow any longer
dynamic instability

31
Q

General mechanism for all G-protein receptors

A

ligand binds to receptor and causes a conformational change on the cytoplasmic side of the plasma membrane which binds and activates G-protein (alpha subunit) by replacing GDP with GTP
Alpha subunit then goes on to react with an enzyme regulated by G protein –> relays the signal from the first message (ligand) to deeper into the cell by producing mediators aka second messengers
The secondary messenger activates a Ser/Thr kinase that phosphorylates proteins (amplifies signal from original primary messenger) which results in a biological response

32
Q

types of receptors

A
  1. g protein receptors
  2. catalytic receptors
  3. intracellular receptors
33
Q

Adenylyl cyclase

A

once the alpha subunit of g protein binds to adenylyl cyclase, ATP gets converted to cAMP which acts as a secondary messenger in the cell
cAMP then goes on to regulate protein kinase A (PKA)
PKA phosphorylates proteins which have biological affects in the cell

34
Q

Aberrant activity of Gs and Gi proteins

A

Cholera - modifies alpha subunit on Gs in intestinal cells which makes it so it cannot be shut off. this results in the overpdn of cAMP and diarrhea and dehydration

Pertussis - modifies Gi in the respiratory tract so it inhibits the alpha subunit from shutting adenylyl cyclase off

35
Q

Phospholipase C

A

regulated by G protein
2 secondary messangers produced: IP3 and DAG(anchored in the membrane)
IP3 then binds to ER to release calcium
Ca and DAG work together as secondary messengers by activating protein kinase c (PKC)
PKC phosphorylates proteins in the same way that PKA does

36
Q

Catalytic receptors

A

3 domains: ligand binding, transmembrane, effector region (within cell)
upon binding of ligand, two receptors form dimers
each receptor tail tyrosine phophorylates the other in the dimer
SH2 (adaptor protein) then is able to bind to the phosphorylated tyrosines

37
Q

Ras

A

homologous to the alpha subunit of G protein
Ras binds to SH2 containing domains that are already bound to the phosphorylated tyrosines
Ras activates the MAP kinase cascade (much longer lived that tyrosine phos.)
Final enzyme: MAP kinase gets phosphorylated and translocates to the nucleus to act as a trxn factor

38
Q

STATs

A

signal transducers and activators of trxn
SH2 containing proteins that can bind directly to the phosphorylated tyrosines (unlike Ras)
STATs get tyrosine phosphorylated and form dimers –> translocate to nucleus to act as trxn factor

39
Q

inhibitors of DNA synthesis

A

5-Fluroruracil

methotrexate

IBSS 501 (2 decks)

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