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STEP 1 (4) > Biochemistry-Cellular > Flashcards

Biochemistry-Cellular Flashcards

1
Q

Describe regulation of the cell cycle

A

Checkpoints control transitions between phases in the cel cycle. This process is regulated by cyclines, cyclin-dependent kinases (CDKs), and tumor suppressors.

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2
Q

What is included in M phase?

A

mitosis (prophase, prometaphase, metaphase, anaphase, and telophase) and cytokinesis

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3
Q

What are the phases of the cell cycle?

A

M - G1 - S - G2 -M

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4
Q

Note that CDKs are constitutive and active,

Cyclins are regulatory proteins that control cell cycle events; are ohase specific, and activate CDKs

Cyclin-CDK complexes phosphorylate other proteins to coordinate cell cycle progression

A
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5
Q

What normally inhibits G1 to S progression?

A

p53 and hypophosphorylated Rb (mutations in these genes can result in unrestrained cell growth (e.g. Li- Fraumeni syndrome)

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6
Q

What are the main cell types?

A

Permanent (remain in Go phase, regenerate from stem cell; neurons, skeletal and cardiac muscle; RBCs)

Stable (enter G1 when stimulated; hepatocytes, lymphocytes)

Labile (Never go to Go, divide rapidly with a short G1; most affected by chemo; bone marrow, gut epithelium, skin, germ cells hair)

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7
Q

What is the rough ER?

A

the site of synthesis of secretory (excreted) proteins and of N-linked oligosaccharide addition to many proteins

Nissl bodies (RER in neurons) synthesize peptide neurotransmitters for secretion

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8
Q

What does the smooth ER do?

A

site of steroid synthesis and detox of drugs and poisons (lacks surface ribosomes)

Liver hepatocytes and steroid hormone producing cells of the adrenal cortex and gonads are rich in SER

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9
Q

Describe cell trafficking

A

The golgi is the distribution center for proteins and lipids from the ER to the vesicles and plasma membrane. The golgi modified N-oligosacchardies on asparagine, adds O-oligosacchardies on serine and threonine, and adds mannose-6-phosphate to proteins for trafficking to lysosomes

Endosomes are the sorting centers for materials from outside the cells or from the SGolgi, sending it to lysosomes for destruction or back to the membrane/Golgi for further use

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10
Q

What is I disease?

A

(inclusion cell disease)- inherited lysosomal storage disorder caused by a defect in N-acetylglucosaminyl-1-phosphotransferase that results in failure of the Golgi to phosphorylate mannose residues (i.e. decreased mannose-6-phosphate) on glycoproteins. This results in proteins that are secreted extracellularly rather than delivered to lysosomes.

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11
Q

How does I disease present?

A

coarse facial features, clouded corneas, restricted joint movement, and high plasma levels of lysosomal enzymes

Often fatal in childhood

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12
Q

What is a signal recognition particle?

A

Abundant, cytosolic ribonucleoprotein that traffics proteins from the ribosome to the RER. Absent or dysfunctional SRP causes proteins to accumulate in the cytosol

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13
Q

What are some major vesicular trafficking proteins?

A

COP1: Golgi to golgi (retrograde) or cis-Golgi to ER

COP2: ER to cis-Golgi (anterograde)

Clathrin: trans-golgi to lysosomes and plasma membrane to endosomes (receptor mediated endocytosis)

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14
Q

What is the role of peroxisomes?

A

Membrane-enclosed organells involved in the catabolism of very-long-chain fatty acids, branched-chain FAs, and AAs

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15
Q

What is the role of proteasomes?

A

These are barrel-shaped protein complexes that degrade damaged or ubiquitin-tagged proteins (defects in this system have been implicated in Parkinson disease)

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16
Q

What are the main cytoskeleton components?

A

Microfilaments (actin; muscle contraction, cytokinesis)

Intermediate filaments (e.g. vimentin, GFAP, desmines, cytokeratin, lamins, neurofilaments; maintain cell structure)

Microtubules (e.g. cilia, flagella, mitotic spindle, neuronal trafficking; movement, and cell division)

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17
Q

What body part does a vimentin stain ID? Desmins? Cytokeratin?

A

Vimentin- Connective tissue

Desmin- Muscle

Cytokeratin- Epithelial cells

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18
Q

What body part does a GFAP stain ID? Neurofilaments?

A

GFAP- Neuroglia

Neurofilaments- neurons

19
Q

Describe the structure of microtubules

A

cylindrical structure composed of a helical array of polymerized heterodimers of a- and b-tubulin. Each dimer has 2 GTP bound.

Microtubules are incorporated into flaggella, cilia, mitotic spindles

20
Q

Anterograde transport along microtubules is accomplished via ______. Retrograde?

A

Anterograde- kinesin

Retro- dynein

21
Q

What drugs act upon microtubules?

A

Microtubules Get Constructed Very Poorly

Mebendazole (antihelminthic)

Griseofulvin (antifungal)

Colchicine (antigout)

Vincristine/Vinblastine

Paclitaxel

22
Q

What is the structure of cilia?

A

9+2 arrangement of microtubule doubles with axonemal dynein, an ATPase that links peripheral 9 doubles and causes bending of cilium by sliding

23
Q

What is Kartagener syndrome (primary ciliary dyskinesia)?

A

immotile cilia due to a dynein arm defect resulting in male and female infertility due to immotile sperm and dysfunctional fallopian tube cilia.

Increased risk of ectopic pregnancy

Can also result in bronchiectasis, recurrent sinusitis, and situs inversus

24
Q

What is the composition of the plasma membrane?

A

asymmetric lipid bilayer containing cholesterol, phospholipids, spingolipids, glucolipids, and proteins

NOTE: Fungal membranes contain ergosterol

25
Q

Describe the NaKATPase

A

3Na+ go out of the cell (when the pump is phosphorylated), 2K+ go in (when the pump is dephosphorylated)

26
Q

What drugs block the NaKATPase?

A

Ouabain inhibits by binding to the K+ sight

Cardiac glycosides (digoxin and digitoxin) directly inhibit, whihc leads to indirect inhibition of Na/Ca2+ exchange to increase intracellular Ca2+ leading to increased cardiac contractility

27
Q

What are the types of collagen?

A

I-IV

28
Q

Describe type I collagen

A

most common (90%)- found in bone (made by osteoblasts), skin, tendons, dentin, fascia, cornea, and is involved in late wound repair

Decreased production in osteogenesis imperfecta type I

29
Q

Describe type II collagen

A

found in cartilage (including hyaline), vitreous body, and nucleus pulposus

30
Q

Describe type III collagen

A

found in reticulin-skin, blood vessels, uterus, fetal tissue, and granulation tissue

Type III is deficient in the uncommon, vascular type of Ehlers-Danlos

31
Q

Describe type IV collagen

A

Found in basement membrane, basal lamina, and the lens

defective in Alport syndrome, and targeted by Abs in Goodpasture syndrome

32
Q

Describe the initial parts of collagen synthesis and structure

A
  1. Synthesis (RER)-translation of collagen a chains (preprocollagen)-usually Glu-X-Y (X and Y are proline or lysine). Glycine content best reflects collagen synthesis (collagen is 1/3 glycine)
    2) Hydroxylation of specific proline and lysine residues (requires vitC; deficiency= scurvy)
33
Q

Describe the parts 3 and 4 of collagen synthesis and structure

A

3) Glycosylation of pro-a-chain hydroxylysine residues and the formation of procollagen via hydrogen and disulfide bonds (triple helix of 3 collagen a chains); Problems forming triple helix= osteogenesis imperfecta
4) Exocytosis of procollagen from fibroblast into extracellular space

34
Q

Describe the parts 5 and 6 of collagen synthesis and structure

A

5) Proteolytic processing-cleavage of disulfide rich terminal regions of procollagen, transforming it into insoluble tropocollagen
6) Cross-linking: Reinforcement of many staggered tropocollagen molecules by covalent lysine-hydroxylysine cross-linkage (by copper-containing lysyl oxidase) to make collagen fibrils; problems with cross-linking= Ehlers-Danlos or Menkes disease

35
Q

Describe osteogenesis imperfecta

A

Genetic bone disorder caused by defects in collagen processing. Manifests with:

mutliple fractures with minimal trauma

blue sclera due to the translucency of the CT over the choroidal veins

hearing loss (abnormal ossicles)

dental imperfections due to a lack of dentin

36
Q

What is Ehlers Danlos syndrome?

A

Disease of faulty collagen syntheis causing hyperextensible skin, tendency to bleed, and hypermobile joints

There are multiple types and inheritance and severity may vary (can be AD or AR)

37
Q

What are some types of Ehlers Danlos syndrome?

A

Hypermobility (most common)

Classical types (joint and skin problems)- caused by mutation in type V collagen

Vascular type (vascular and organ rupture)-deficient type III collagen

38
Q

What is Menkes disease?

A

X-linked recessive CT disease caused by impaired copper absorption and transport due to a defective Menkes protein (ATP7a) leading to decreased activity of lysyl oxidase resulting in brittle, kinky hair, growth retardation, and hypotonia

39
Q

What is elastin?

A

stretchy protein within skin, lungs, large, arteries, elastic ligaments, vocal cords, and ligamenta flava

40
Q

What is the composition of elastin?

A

rich is nonhydroxylated proline, glycine, and lysine residues

41
Q

Elastin is normally broken down by _______

A

elastase (which is inhibited by a1-antitrypsin

42
Q

What causes Marfan syndrome?

A

defct in fibrillin, a glycoprotein that forms a sheath around elastin

43
Q

What causes wrinkling of skin with age?

A

decreased collagen and elastin production

STEP 1 (4) (18 decks)

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