front 1 taxis | back 1 the movement of an organism in response to a stimulus |
front 2 positive taxis | back 2 towards a stimulus |
front 3 negative taxis | back 3 away from a stimulus |
front 4 chemotaxis | back 4 the movement in response to chemicals (e.g. bacteria with flagella away from repellants or to nicer locations, neutrophils in humans with infection) |
front 5 short-range cell-signaling | back 5 affects only nearby cells |
front 6 long-range cell-signaling | back 6 affects cells throughout the organism |
front 7 ligands | back 7 signaling molecules that bind to receptors to trigger a response by changing the shape of the receptor protein |
front 8 ligand-gated ion channels | back 8 receptor that opens or closes an ion channel upon binding with a particular ligand |
front 9 What are some examples of ligand-gated ion channels? | back 9 on skeletal muscle cells that open with acetylcholine; when sodium depolarizes muscle cells they contract |
front 10 catalytic (enzyme-linked) receptors | back 10 enzymatic active site on cytoplasmic side of membrane (e.g. insulin receptors) |
front 11 G-protein-linked receptor | back 11 no act as an enzyme, binds to GTP or GDP on intracellular side when a ligand is bound extracellularly |
front 12 What is an example pf a G-protein linked receptor? | back 12 cAMP hunger signal activates the secondary messengers of epinephrine and glucagon |
front 13 phosphorylation cascades | back 13 series of protein kinases add a phosphate group to the next protein in a cascade sequence, helps amplify signal, quickly turn response on or off |
front 14 signal transduction in bacterial cells | back 14 usually a simpler two-component regulatory system in transduction pathways |
front 15 signal transduction pathways can change stuff | back 15 cell's phenotype, apoptosis, mutations in receptor or ligand, drugs / chemicals inhibit or excite parts of pathway |
front 16 negative feedback pathway (feedback inhibition) | back 16 when a metabolic reaction turns itself off using its own end product |
front 17 cell communication in plants | back 17 signals in response to environmental stimuli, light receptors, chemical communication, between plants |
front 18 non-dividing cells | back 18 often highly specialized cells created from a population of less specialized cells |
front 19 temporarily non-dividing cells | back 19 enter G0 phase, where they stay until they get a signal to reenter the normal cell cycle |
front 20 cell cycle | back 20 an orderly sequence of events that extends from when 2 daughter cells form to when they divide again |
front 21 interphase | back 21 majority of cell cycle, metabolic activity = very high, chromosomes duplicated in S phase |
front 22 G1 (growth 1) | back 22 before DNA synthesis begins, enzymes for S phase made (i.e. DNA helicase, DNA polymerase, DNA ligase), regular activity resumes, increased protein / organelle |
front 23 S (DNA synthesis) | back 23 main part of chromosome duplication, DNA copied into sister chromatids |
front 24 G2 (growth 2) | back 24 DNA synthesis completion, prepare for cell division, protein synth increased for proteins needed for cell division |
front 25 mitotic (M) phase | back 25 most dramatic appearance changes, PMAT and cytokinesis |
front 26 skin, digestive tract lining cells divide... | back 26 frequently, constantly sloughed off = must be regenerated |
front 27 liver cells divide... | back 27 only if damaged (cell division repairs wounds) |
front 28 nerve and muscle cells divide... | back 28 never |
front 29 anchorage dependency | back 29 plant/animal cells must be anchored to a surface to divide (free-floating cells rarely divide) |
front 30 density dependent inhibition | back 30 cells multiply to form single layer and stop dividing when touch each other because of inadequate growth factor supply |
front 31 growth factors proteins | back 31 secreted by certain body cells, stimulate cells nearby to divide (more densely packed cells = more use up growth factors = divide slower) |
front 32 cell cycle control system | back 32 cyclically operating set of proteins in the cell that trigger and coordinate major cell cycle events, from environmental conditions outside cell or go signals inside cell |
front 33 cell cycle checkpoints | back 33 end of G1 (MOST IMPORTANT AS PREVENTS S PHASE) AND NON-DIVIDING STATE, end of G2 (prevents prophase / mitotic phase), metaphase (stops if not all chromosomes are attached to mitotic spindle on M plate) |
front 34 cyclin dependent kinases (CDKs) and cyclins | back 34 bind to form a complex that causes the cell cycle to continue, regulated by checkpoints to control progression |
front 35 carcinoma | back 35 cancer of external / internal body coverings (e.g. skin, intestinal lining) |
front 36 sarcomas | back 36 cancer of supporting tissues (e.g. bone and muscle) |
front 37 leukemias and lymphomas | back 37 cancers of blood-forming tissues (e.g. bone marrow, spleen, lymph nodes) |
front 38 oncogenes | back 38 mutated genes that induce cancer, normally for proper cells growth and CCCS, but convert normal cells into cancerous cells due to mutated genes |
front 39 proto-oncogene | back 39 normal healthy version of a gene |
front 40 tumor suppressor genes | back 40 produce proteins that prevent the conversion of normal cells into cancer cells, detect damage in the cell, use CDK / cyclin complexes to stop cell growth until damage repaired |
front 41 cancer causes | back 41 oncogenes (speed up cycle), tumor suppressors (remove stop checkpoints) |
front 42 chemotherapy | back 42 antimitotic drugs disrupt cell division for whole body (vinblastine, taxol), fewer side effects |
front 43 radiation therapy | back 43 direct to tumor high-energy radiation that disrupts division |