Cell junctions Flashcards
Q: What are the two major types of inputs that elicit signals in a cell?
A: 1. Contact-dependent signals – require direct contact between cells (e.g. cadherins, integrins).
2. Diffusible signals – use molecules like hormones or gases that diffuse to target cells.
Q: What are examples of specialized cell inputs not classified as contact or diffusible?
A: Light, heat, mechanical deformation.
Q: What are cadherins and their function?
A: A family of adhesion proteins important for cell-cell adhesion, crucial in tissue formation and maintenance.
Q: What intracellular structures do cadherins connect to?
A: They connect to actin cytoskeleton via catenins.
Q: What are gap junctions composed of and what is their function?
A: Made of connexins, they allow direct cytoplasmic communication for ions and small molecules between adjacent cells.
Q: Name two clinical conditions associated with gap junction defects.
A: 1. Cx26 mutations – congenital deafness
2. Cx32 mutations – Charcot-Marie-Tooth disease
Q: How do integrins mediate signalling?
A: By binding extracellular matrix (ECM) components, causing dimerization, activating proteins like talin, paxillin, and focal adhesion kinase (FAK) which remodel the cytoskeleton.
Q: What is the Ephrin pathway?
A: A contact-dependent signal involving ligand-receptor pairs (Eph-Ephrin) across cells, triggering cytoskeletal remodelling and gene expression.
Q: What are the three main types of receptor-mediated signalling?
A: 1. Ion channel-linked receptors (e.g. nicotinic ACh, GABA-A)
2. G-protein coupled receptors (GPCRs)
3. Enzyme-linked receptors (e.g. insulin receptor)
Q: How do peptide and lipid hormones differ in receptor location?
A: Peptides bind surface receptors; lipids (e.g., steroids) typically bind intracellular receptors
Q : Describe the GPCR pathway using muscarinic receptors as an example.
A: Ligand binds GPCR → activates G protein (e.g., Gq) → stimulates phospholipase C → generates IP3 → triggers Ca²⁺ release.
Q: How does insulin signalling work via tyrosine kinase receptors?
A: Insulin binds → receptor dimerizes → activates PI3K → AKT pathway → promotes GLUT4 translocation and gene transcription.
Q: How does nitric oxide (NO) function as a signalling molecule?
A: NO diffuses to nearby smooth muscle → activates guanylyl cyclase → increases cGMP → causes vasodilation.
Q: Can glucose act as a signalling molecule? Why?
A: Yes. It enters beta cells via GLUT transporters, triggering metabolic and calcium signalling cascades, leading to insulin secretion.
Q: What role do cell junctions play in cancer?
A: Breakdown of cell-cell adhesion (e.g., cadherins) leads to epithelial-mesenchymal transition (EMT), aiding metastasis.
Q: What is insulin resistance, and why is it clinically significant?
A: A condition where cells don’t respond to insulin, even when it’s present. It’s central to type 2 diabetes, and involves defects in insulin receptors or downstream signalling pathways (e.g., AKT).
