Biochemistry- Celular Flashcards
Cell cycle phases
M phase (shortest phase of cell cycle) includes mitosis (prophase, prometaphase, metaphase, anaphase, telophase) and cytokinesis. G1 and G0 are of variable duration.
Cyclins
Regulatory proteins that control cell cycle
events; phase specific; activate CDKs.
Tumor suppressors
p53 induces p21, which inhibits CDKs
Rb inhibition of G1-S progression
Cyclin-CDK complexes
Phosphorylate other proteins to coordinate
cell cycle progression
CELL TYPES (according to cell cycle)
Permanent (remain G0)
Stable (quiscent) (enter to G1 from G0)
Labile (Never G0, dived rapidly)
Rough endoplasmic
reticulum
Site of synthesis of secretory (exported) proteins.
Nissl bodies (RER in neurons)
Free ribosomes
Smooth endoplasmic
reticulum
Site of steroid synthesis and detoxification of
drugs and poisons
I-cell disease (inclusion cell disease/mucolipidosis type II)
inherited lysosomal storage disorder; defect in N-acetylglucosaminyl-1-phosphotransferas.
clinical features of I-cell disease
Coarse facial features, clouded corneas, restricted joint movement, and high plasma levels of lysosomal enzymes. Often fatal in childhood
N-acetylglucosaminyl-1-phosphotransferase
Golgi to phosphorylate mannose residues on glycoproteins, proteins are to lysosomes.
Vesicular trafficking proteins
“Two (COPII) steps forward (anterograde); one
(COPI) step back (retrograde).”
Clathrin: trans-Golgi lysosomes; plasma
membrane endosomes
Peroxisome
Catabolism of very-long-chain fatty acids (through
β-oxidation), branched-chain fatty acids, amino acids, and ethanol.
Peroxisomal disorders
Zellweger syndrome
Refsum disease
Refsum disease
scaly skin, ataxia, cataracts/night blindness, shortening of 4th toe, epiphyseal dysplasia.
Zellweger syndrome
hypotonia, seizures, hepatomegaly, early death
Proteasome
degrades damaged or ubiquitin-tagged proteins.
Microfilaments
Actin, microvilli
Intermediate
filaments
Vimentin, desmin, cytokeratin, lamins, glial
fibrillary acid proteins (GFAP), neurofilaments.
Microtubules
Cilia, flagella, mitotic spindle, axonal trafficking,
centrioles
Drugs that act on microtubules (Microtubules
Get Constructed Very Poorly)
Mebendazole (antihelminthic) Griseofulvin (antifungal) Colchicine (antigout) Vincristine/Vvinblastine (anticancer) Paclitaxel (anticancer)
Immunohistochemical stains for intermediate filaments
Vimentin (mesenchymal tissue) Desmin (muscle) Cytokeratin (epithelial cells) GFAP (neuroglia) Neurofilaments (neuron)
Cilia structure
- 9 doublet + 2 singlet arrangement
- Basal body 9 microtubule triplets
- Axonemal dynein—ATPase that links peripheral
9 doublet
Kartagener syndrome
1° ciliary dyskinesia:
- disminution fertility due to immotile sperm and dysfunctional fallopian tube cilia.
- bronchiectasis, recurrent sinusitis, chronic ear infections
- Conductive hearing loss
- Situs inversus
Sodium-potassium
pump
3Na+ go out of the cell (pump phosphorylated) and 2K+ come into the cell (pump dephosphorylated)
Ouabain
Cardiac glycosides
- inhibits by binding to K+ site.
- directly inhibit the Na+-K+ ATPase
Types of collagen
Be (So Totally) Cool, Read Books.
I: Bone, Skin, Tendon (osteogenesis imperfecta I)
II: Cartialge
III: Reticuline (vascular ehlers-danlos)
IV: Basement membrane (alport, goodpasteur)
Osteogenesis imperfecta
autosomal dominant COL1A1 o COL1A2 Patients can’t BITE: Bones = multiple fractures I (eye) = blue sclerae Teeth = dental imperfections Ear = hearing loss
Ehlers Danlos
- Hypermobility type (joint instability): most common type.
- Classical type (joint and skin symptoms): caused
by a mutation in type V collagen. - Vascular type (vascular and organ rupture): deficient type III collagen.
Menkes disease
- X-linked recessive
- impaired copper absorption and transport due to defective Menkes protein (ATP7A).
- brittle, “kinky” hair, growth retardation, and hypotonia.
Marfan syndrome
- autosomal dominant
- affecting skeleton, heart, and eyes.
- FBN1 gene mutation on chromosome 15 results in defective fibrillin
