ex16v Flashcards
How do transcription factors interact with DNA?
Transcription factors interact with DNA through structural motifs such as helix-turn-helix, zinc finger, or leucine zipper domains, which fit into the DNA’s major groove and form specific interactions via hydrogen bonds, ionic bonds, and hydrophobic contacts.
How can transcription factors’ specificity and affinity to DNA be increased?
Transcription factors increase specificity and affinity by forming homo- or heterodimers, recognizing longer sequences, or cooperating with other factors and chromatin remodeling complexes, expanding their regulatory potential.
How does nucleosome structure affect transcription factor binding?
Nucleosomes compact DNA, reducing accessibility. Transcription factors bind transiently during nucleosome “breathing” or use remodeling complexes like SWI/SNF and histone acetylation to expose DNA for transcription machinery.
What are G-protein coupled receptors?
GPCRs are the largest family of plasma membrane receptors in humans, mediating signals from extracellular stimuli like hormones, neurotransmitters, and sensory inputs.
How do GPCRs mediate signals via phospholipids?
Ligand binding activates G-proteins, which stimulate phospholipase C (PLC) to cleave PIP2 into IP3 and DAG. IP3 triggers Ca²⁺ release, while DAG activates protein kinase C, driving downstream signaling.
How does Ca²⁺ regulate enzyme activity and protein function?
Ca²⁺ binds to proteins like calmodulin, activating enzymes such as CaMKs, or works with DAG to activate PKC, modulating cellular functions like secretion and motility.
How are Ca²⁺ levels in cells regulated?
Ca²⁺ levels are regulated by ion channels, pumps like SERCA, and buffers like calbindin. Positive feedback amplifies Ca²⁺ release, while negative feedback prevents excessive signaling, creating Ca²⁺ waves.
How do receptor tyrosine kinases activate Ras and affect gene expression?
Ligand-bound RTKs dimerize and autophosphorylate, recruiting adaptor proteins like GRB2 and SOS, which activate Ras by exchanging GDP for GTP. Active Ras initiates the MAPK cascade, leading to transcriptional changes.
How do mutations in Ras and other genes contribute to colorectal carcinoma?
Mutations in Ras lock it in an active state, driving proliferation. APC mutations disrupt Wnt signaling, p53 loss impairs apoptosis, and PI3K/PTEN mutations enhance survival, collectively promoting tumor progression.
What is apoptosis, and how do extracellular signals induce it?
Apoptosis is a programmed cell death mechanism where extracellular signals like Fas ligand bind death receptors, forming DISC, which activates caspase-8 and downstream caspases, leading to DNA fragmentation and cell disassembly.
How do survival factors inhibit apoptosis?
Survival factors upregulate anti-apoptotic proteins like Bcl-2 to prevent cytochrome c release or phosphorylate and inactivate pro-apoptotic proteins like BAD via AKT signaling.
How does DNA damage induce apoptosis?
DNA damage activates p53, which upregulates pro-apoptotic proteins like Bax, permeabilizing mitochondria to release cytochrome c. Cytochrome c activates the apoptosome, triggering caspase-mediated apoptosis.
What is RNA editing?
RNA editing modifies RNA sequences post-transcriptionally, such as A-to-I or C-to-U changes, diversifying protein function.
What is a GTPase activating protein (GAP)?
GAPs enhance GTP hydrolysis in G-proteins, inactivating them and terminating signaling.
What is a cancer stem cell?
A cancer stem cell is a tumor cell capable of self-renewal, driving tumor growth and recurrence.
