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A researcher studying neuron development should choose which model organism?
D. melanogaster (fruit fly)
If a GABAA receptor mutation reduces Cl⁻ influx, how would neurons likely behave?
Depolarized (more excitable)
Why might Rab3GAP1 knockout flies help study Warburg Micro Syndrome?
Flies share conserved RAB18 pathway genes.
If lymphocytes incorporate more radiolabeled T nucleotides post-infection, this suggests:
Lymphocytes divide faster (DNA synthesis increases)
(Increased T uptake indicates DNA replication for proliferation)
If chromosomes fail to attach to the spindle, cells arrest in:
metaphase
(M checkpoint halts metaphase until all chromosomes attach)
Why does a nonsense mutation often cause loss of protein function?
It introduces a premature stop codon, truncating the protein
eg Rab3GAP1 nonsense mutations in WMS
Enhancers regulate gene expression by
Binding proteins to increase transcription
Myelin sheaths in the CNS are produced by
oligodendrocytes
During an action potential, depolarization is caused by
Na⁺ influx
Multiple sclerosis results from
Myelin degradation in the CNS
(autoimmune attack on oligodendrocytes disrupts signaling)
Cl⁻ influx typically causes
hyperpolarization
Glutamate primarily binds to receptors that allow influx of
Na⁺ and Ca²⁺
(AMPA/NDMA receptors depolartize postsynaptic neurons (EPSPs)
Botulinum toxin inhibits synaptic transmission by
preventing vesicle fusion
Temporal summation occurs when
A single synapse fires rapidly in succession
During metastasis, cancer cells can extravasate from the bloodstream into tissues. What is required for this process?
protease activity
How does protease activity facilitate metastasis?
By breaking down extracellular matrix components
A key feature of apoptosis that distinguishes it from necrosis is that apoptosis
Is a controlled, energy-dependent process
A lymphoma patient is found to overexpress Bcl-2. The most likely effect of this overexpression is
Inhibition of programmed cell death
The BRCA-1 gene is a tumor suppressor because it:
Helps repair DNA double-strand breaks
Tumor suppressor genes function by
Enhancing apoptosis and inhibiting uncontrolled growth
how does the BCR-ABL fusion protein promotes leukemia?
It acts as a constitutively active tyrosine kinase