MTM WK2 - FUNDAMENTAL CELL PROCESSES Flashcards
CATABOLIC PATHWAY
breaks complex muscle to simple muscle (releases energy)
ANABOLIC PATHWAY
builds complex muscle from simple muscle (uses ATP)
GLYCOLYSIS YIELD
glucose = 2 pyruvate
2 NAD+ = 2NADH
2ADP = 2ATP
GLYCOLYSIS PROCESS
glucose converted to fructose1-6-biphosphate (uses 2 ATP) which is split into glyceraldehyde-3-phosphate which is coverted to pyruvate by pyruvate
ANAEROBIC RESP.
pyruvate converted to lactate by pyruvate dehydrogenase which reforms NAD+ from NADH (as NAD+ needed for glycolysis)
CORI CYCLE (GLUCONEOGENESIS)
- lactate moved to liver & converted to glucose for respiration
- (2ATP to ADP) (NADH to NAD+) (GTP to GDP)
PYRUVATE DECARBOXYLATION
pyruvate converted to acetyl-CoA & CO2 by pyruvate dehydrogenase (PDH) (NAD+ to NADH)
PDH ENZYME REGULATION
- activated by calcium (CA2+ + H2O = Pi (activates enzyme)
- inactivated by NADH activating the kinase enzyme
TCA YIELD
- acetyl CoA = CoA + 2CO2
- 3NAD+ = 3NADH (B3)
- FAD = FADH2 (B2)
- GDP + Pi = GTP
- after TCA, there are 10 NADH (each make 2.5 ATP) & 2 FADH2 (each make 1.5 ATP)
ELECTRON TRANSFER CHAIN (ETC)
- NADH (to compex1) & FADH (to complex 2) transfer high energy electrons to ETC
- NADH oxidised to release 1 proton & 2 electrons (2 e- transport 4 protons)
- electrons lose energy to each carrier (used to AT protons from matrix to intermembrane space)
- way more H+ in intermembrane than matrix so pass down ATP synthase channel to form ATP (3 H+ = 1 ATP) (+ 1 more H+ to move ATP to cytosol)
- electrons + protons added to O2 (terminal acceptor) to form H2O (cyanide can inhibit complex 4 to stop O2 accepting electrons)
GLYCEROL PHOSPHATE SHUTTLE (GPS)
NADH made in glycolysis is in cytosol but can only be oxidised in mitochondria (BUT can’t cross membrane) so GPS uses it to form glycerol-3-phosphate which diffuses into mitochondria & forms FADH2)
UNCOUPLED TRANSPORT IN BROWN ADIPOSE TISSUE
protons pass from intermembrane space to matrix alone (not through ATP synthase channels) through uncoupling proteins so no ATP forms (energy lost as heat (good to maintain body temp)
WARBURG EFFECT IN CANCER
tumour cells undergo aerobic glycolysis which produces lots of metabolism which favours rapid proliferation of cell so there is rapid tumour growth (do glycolysis instead of oxidative phosphorylation even tho there is oxygen)
MALATE/ASPARTASE SHUTTLE
- malate dehydrogenase converts OAA to malate (to be transported into mitochondria) (NADH to NAD+)
- malate reconverted back to OAA by malate dehydrogenase (NAD+ to NADH)
- OAA can’t cross mitochondria so converted to aspartate which crosses back into cytosol & is reconverted back to OAA by mitochondrial malate dehydrogenase
- MALATE ASPARTATE function is to get NADH into mitochondria (broken to NAD+ when making malate but reforms NADH in mitochondria later)
BENEFITS OF BASAL SIDE OF EPITHELIAL CELL
- allows cell to receive nutrition from arterial supply
- enables cell to receive sensory supply
TYPES OF EPITHELIAL TISSUE (layers)
SIMPLE (every cell rests on basal lamina (1 layer of cells))
STRATIFIED (cells arranged in layers on top of one another & only lowest layer is on basal lamina)
PSEUDOSTRATIFIED (single layer of irregularly shaped cells where all rest directly on basal lamina but cells are irregularly shaped so look like many layers not just one)
LOOK AT ALBUM ON LOCATIONS OF DIFFERENT TYPES OF EPITHELIUM
SQUAMOUS - flat (central nucleus)
COLUMNAR - longer than it is wide (nucleus near base)
CUBOIDAL - cube shape (central nucleus)
TRANSITIONAL - can differentiate e.g. bladder stretching
EPITHELIA WITH MICROVILLI
microvilli are in membrane and ACTUALLY BEND THE apical surface of MEMBRANE which increases SA for absorptive surface
EPITHELIA WITH CILIA
anchor on top of apical surface of membrane to waft away fluids (sit right above goblet cells so waft away mucous made by goblet)
KERATINISED EPITHELIUM
dead cells (cells at basal have nutrients but as you rise, less likely to live so the dead basal cells pushed up when new ones form which leaves a protective layer above epithelium)
CELL JUNCTIONS
- TIGHT JUNCTIONS (found at apical region & stop molecules passing through intercellular space)
- ADHESIVE BELT (anchors adjacent cells)
- DESMOSOMES (main junction for binding cells together)(on sides)(hemidesmosomes at basal side to bind to connective)
- GAP JUNCTIONS (passageway between adjacent cells to let small molecules move between neighbouring cells)
- CARRIER MOLECULES BETWEEN ADJACENT CELLS
METAPLASIA
reversible conversion of one differentiated cell type to another
NEOPLASIA
abnormal & excess growth of tissue (cancer)
DYSPLASIA
abnormal development of cells in tissue/organ (not cancer yet)
HOW TO NAME EPITHELIUM
- simple or compound
- shape of upper layer
- epithelium
CELL CYCLE STAGES
- G1 (growth & DNA rep.)
- S (DNA rep.)
- G2 (growth)
- M (mitosis)
G1 CHECKPOINT
ensures cell large enough to divide & enough nutrients for daughter cells (no go-ahead signal = cell enters non-dividing state (G0)
G2 CHECKPOINT
ensures DNA rep. in S phase completed successfully (looks for damaged DNA)
METAPHASE CHECKPOINT
ensures all chromosomes are attached to mitotic spindle
KINASE PROTEIN
protein which activates/deactivates another protein by phosphorylating them
CYCLIN-DEPENDENT KINASE (CdK)
- drive checkpoints
- stays in cell as inactive form until activated by cyclin
PRODUCTION OF CYCLIN
also look at cyclin graph on phone
accumulates during different stages of cycle but by G2, there is enough cyclin available to form M-CdK (initiates mitosis but is switched off in process that destroys cyclin after mitosis)
WAYS CELLS CAN BECOME ONCOGENIC
- receptor mutates so is always active = deregulated cell production
- signalling G-protein mutates so is always active = deregulated cell production
- regulatory proteins mutate so over expression of transcriptional factor
P53 GENE
- regulates G1/S phase
- DNA damage = higher level of P53 = activates transcription of CdK inhibitor
CONSEQUENCES OF CHECKPOINT FAILURE
- cells produced even in absence of growth factor
- replication of damaged DNA
- division of cells with wrong number of chromosomes
GROWTH FACTOR
- stimulates cell division
- they target receptors to activate G1-CdK which phosphorylates pRB so releases TF regulators (activate genes for cell cycle)
GF SIGNALLING PATHWAY
receptor = RAS protein (g-protein) = kinase cascade (kinase 1 activates kinase 2 etc) = gene regulatory protein form = response
RESTRICTION POINT
- regulated by retinoblastoma protein (tumour-suppressor which is activated by CdK which phosphorylate retinoblastoma protein when GF present & retinoblastoma detaches from transcription regulators so transcription occurs (no GF = retinoblastoma attaches to transcriptin regulators so no mitosis happens)
- point in G1 checks if GF present before starting mitosis
4 stages where ATP made in glycolysis
- glucose -> gluocse-6-phosphate (hexokinase)
- fructose 1,6 biphosphate -> fructose-6-phosphate (phosphofructokinase)
- 1,3-biphosphoglycerate -> 3-phosphoglycerate (phosphoglycerate kinase)
- phosphoenolpyruvate -> pyruvate (pyruvate kinase)
