Final Review Exam 2 Flashcards
GTP is used in translation when:
An AA is added, when a EF is added, and when the ribosomal complex disasociates.
Termination and STOP codons
Ribosome recognized STOP codon, RFs bind to the A site and cleave the polypeptide.
Prokaryotic Elongation Inhibitors mechanisms of action:
Tetracycline: bind smal SU and block entry of AA-tRNA.
Chloramphenicol: inhibits peptidyl transferase.
Clindamycin and erythromycin: binds to large SU and blocks translocation of ribosome.
Streptomycin: binds to small SU and interferes with the binding of fmet-tRNA.
Eukaryotic Elongation Inhibitors mechanisms of action:
Cyclohexamide: inhibits peptidyl transferase.
Diphtheria toxin: inactivates eEF-2.
Shiga toxin and Ricin: binds to large SU and blocks entry of AA-tRNA.
Secretory pathway signals (4)
ER lumen: KDEL
Secretory vesicle: Trp-rich domain.
Lysosome: Mann 6-P
CM: N terminal apolar
Cytoplasmic pathway signals (3)
Mitochondria: N term a-helix
Nucleus: Lys Arg rich
Peroxisome: SKL
Mechanism of AD
APP breaksdown to amyloid beta peptide (AB). AB forms plaques in brain
Mechanism of PD
a-synuclein aggregates to form Lewy bodies. Causes death of dopaminergic neurons in substantia negra.
Mechanism of HD
Huntington gene is mutated resulting in CAG repeats, causing poly-Gln. Causes selective death of cells in basal ganglia.
GEF, GTPase and GAP
GEF causes ADP –> ATP
GTPase does opposite
GAP stimulates GTPase
Gq pathway
GTP –> PLC –> DAG, IP3
IP3 –> Ca 2+ (2nd messenger) –> PKC
Viagra mechanism
Inhibits cGMP PDE
Increases cellular cGMP –> smooth muscle relaxation, vasodilation.
NO mechanism
Activates guanylate cyclase
GMP –> cGMP (smooth muscle relaxation and vasodilation).
Cholera and Pertussis
Cholera: prevents inactivation of Gs (AC always on)
Pertussis: prevents activation of Gi (AC not inhibited).
GRKs
Phosphorylate GPCR. Arrestin binds and inactivates GPCR.
Reciprocal and Robertsonian transocations
Reciprocal: exchange of material between nonhomologues
Robertsonian: Long arm of 2 chromosomes combined. Short arm lost.
Imprinting
Silencing of a gene.
If a gene is “paternally imprinted”, the paternal gene is silenced.
These are reset after meiosis in each generation.
Same genotype but multiple phenotypes:
Pleiotropy (PKU)
Multiple genotypes but single phenotype:
Ex: CF
Penetrance
Frequency a gene manifests itself
Rb
Expressivity
Variation in phenotype
E2F drives the expression of which cyclins?
A and E (G1 to S)
CDK2 function
Hyperphosphorylates Rb (making it inactive) and activates E2F.
APC/C function
Degrade cyclins in progression from metaphase to anaphase. APC/C ubiquinates S and M cyclins targeting them for degredation.
CDC20
Activates APC/C
MDM2
Keeps p53 inactive via degredation. p53 gets phosphorylated to become active.
p21 function:
Main target for p53, but mainly acts on inhibiting CDK2 (to inactivate E2F)
Hallmarks of cancer (6)
SEAEIR
- self-sufficient in growth signals
- evading growth suppressors.
- activating invasion and metastasis.
- enabling replicative immortality.
- inducible angiogenesis.
- resisting cell death.
HPV
E6 + p53 —> p53 degredation
E7 + Rb —> displaces E2F, E2F active
Taxol
Colchicine
Vinblastine
Drugs that affect microtubules
Taxol: binds and stabilized microtubules.
C & V: binds tubulin dimers and prevents polymerization.
Phalloidin
Cytochalasin
Latrunculin
Drugs that affect actin
Phalloidin: binds and stabilized f-actin
Cytochalasin: caps filaments, preventing polmerization
Latrunculin: binds actin monomers and prevents polymerization
Adherens junctions
Type: cell-cell
CAM: cadherins
Attachment: actin
Function: shape, tension, signaling
Desmosomes
Type: cell-cell
CAM: cadherins
Attachment: intermediate filaments
Function: strength
Hemidesmosomes
Type: cell-matrix
CAM: integrin
Attachment: intermediate filaments
Function: shape, rigidity, signaling
Tight junctions
Type: cell-cell
CAM: N/A
Attachment: actin
Function: solute flow
Gap junctions
Type: cell-cell
CAM: N/A
Attachment: adapters to other junctions
Function: communication, small molecule transmission
Hereditary hemochromatosis
Organ dysfunction due to iron overload.
Why is RBC production dependent on folate and cobalamin?
They are needed for DNA synthesis in the bone marrow.
Deficiency of cobalamin and/or folate can cause?
Megaloblastic anemia
Pernicious anemia
Form of megaloblastic anemia from cobalamin deficiency.
Neutrophils
Multi-nucleated
Acute inflammation and injury; function in bacterial infections.
Contain 3 granules.
Undergo diapedesis.
Eosinophils
Bi-nucleated
Parasitic infections, chronic inflammation and allergies.
Basophils
Hard to see nucleus.
Hypersensitivity and anaphylaxis.
Monocytes
Heart-shaped nucleus, but large cell.
Becomes macrophage.
Lymphocytes
Large nucleus.
HbS mutation and chromosome
b-globin
Glu –> Val
Chromosome 11
Pathophysiology of acute splenic sequestration in HbS
Sickle cells cause vaso-occlusion.
Elevated reticulocyte count.
Enlarging spleen (asplenia)
Acute chest syndrome in HbS
Infection (infiltrate on CXR)
Causes infarction.
Kids w/ HbS are at risk of what infections? (DMS)
- Dactylitis
- Mycoplasma
- Strep pneumoniae
ALA synthase requires:
Vit B6
Porphyrias (4)
- Acute intermittent: PBG demainase
- Congenital erythropoetic: uroporphyrinogen III synthase
- PCT: Uroporphyrinogen decarboxylase
- Variegate: protoporphyrinogen IX oxidase
Pre hepatic Jaundice
Increased unconjugated BR.
Eveyrthing else is fine, just overwhelmed.
Intra hepatic
Impaired uptake, conjugation or secretion of conjugated BR.
Liver is sick (cirrhosis, hepatitis, C-N, Gilbert)
Increased ALT, AST.
Conjugate BR in urine.
Post hepatic
Cannot excrete BR.
Blockage in live/bile duct.
Pale stool, conjuated BR in urine (causing a dark tint).
