exMock Flashcards

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1
Q

Describe mechanisms by which transcriptional regulators are activated or inhibited.

A

Transcriptional regulators are activated by phosphorylation (e.g., CREB), ligand binding (e.g., glucocorticoid receptor), or dimerization (e.g., NF-κB). They are inhibited by repressor binding (e.g., LacI), histone deacetylation, or chromatin remodeling.

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2
Q

Explain the concept of cell memory and how it is maintained across cell divisions.

A

Cell memory is maintained through epigenetic modifications like DNA methylation (e.g., CpG islands) and histone modifications (e.g., H3K27me3 for repression). Positive feedback loops reinforce transcriptional states.

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3
Q

Outline the role of non-coding RNAs in gene expression regulation.

A

miRNAs inhibit translation by binding the 3’ UTR (e.g., let-7 and Ras), siRNAs degrade mRNA via RISC, and lncRNAs scaffold chromatin modifiers (e.g., Xist for X-inactivation).

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4
Q

Compare activation mechanisms of GPCRs and RTKs.

A

GPCRs activate via ligand binding, conformational change, and G-protein activation (e.g., β-adrenergic receptor). RTKs activate through ligand-induced dimerization and autophosphorylation (e.g., EGFR).

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5
Q

Explain the role of second messengers in intracellular signaling.

A

cAMP activates PKA to regulate glycogen metabolism, while Ca²⁺ binds calmodulin to activate kinases like CaMKII. Both amplify signals.

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6
Q

Describe the JAK-STAT pathway and its regulation.

A

Cytokine binding triggers JAK phosphorylation, STAT dimerization, and nuclear translocation. Regulation occurs through SOCS proteins and phosphatases to prevent excessive signaling.

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7
Q

Describe the phases of the cell cycle and their checkpoints.

A

G1 phase involves cell growth, G1/S checkpoint ensures DNA integrity. S phase is DNA replication, G2 phase prepares for mitosis, G2/M checkpoint verifies DNA replication. The M phase involves mitosis and cytokinesis, the spindle checkpoint ensures chromatid alignment.

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8
Q

Discuss the role of cyclin-dependent kinases (Cdks) and cyclins in cell cycle progression.

A

Cdks are activated by binding cyclins (e.g., Cdk1-cyclin B for mitosis). Their activity is regulated by phosphorylation and CKIs like p21.

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9
Q

Outline the role of APC/C in mitosis.

A

APC/C ubiquitinates securin, activating separase to cleave cohesin and separate sister chromatids during anaphase.

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10
Q

Explain actin filament nucleation and treadmilling.

A

Actin nucleation involves Arp2/3 for branched filaments and formin for unbranched filaments. Treadmilling is ATP-actin polymerization at the barbed end and ADP-actin depolymerization at the pointed end.

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11
Q

Describe microtubule structure and function in intracellular transport.

A

Microtubules are hollow tubulin dimers with dynamic instability. Kinesins move cargo to the + end, and dyneins transport to the − end.

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12
Q

Discuss how Rho and Rac regulate cell movement.

A

Rho promotes stress fiber formation for contraction, while Rac stimulates lamellipodia formation for forward movement.

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13
Q

Differentiate between apoptosis and necrosis.

A

Apoptosis involves membrane blebbing, caspase activation, and DNA fragmentation. Necrosis causes cell swelling, membrane rupture, and inflammation.

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14
Q

Describe the intrinsic pathway of apoptosis.

A

Pro-apoptotic proteins Bax and Bak form mitochondrial pores, releasing cytochrome c, which forms the apoptosome with Apaf-1 to activate caspase-9 and initiate apoptosis.

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15
Q

Explain the extrinsic pathway of apoptosis.

A

Death receptors (e.g., Fas) bind ligands, activating caspase-8. This pathway is essential for immune regulation, removing infected or cancerous cells.

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16
Q

Explain the roles of morphogens and lateral inhibition.

A

Morphogens establish gradients for cell fate (e.g., Sonic Hedgehog). Lateral inhibition via Notch-Delta signaling ensures distinct cell fates in neighboring cells.

17
Q

Describe how asymmetric cell division determines cell fate.

A

Unequal distribution of fate-determining factors during division results in daughter cells with different fates (e.g., C. elegans P cells).

18
Q

Discuss how mutations in Hox genes affect development.

A

Hox gene mutations disrupt segment identity, causing developmental abnormalities (e.g., Antennapedia mutation in Drosophila).