Aldol condensation Ox + AcCoA + H2O / Citrate synthase -> Citrate + CoA-SH irreversible

Dehydration Citrate /Aconitase -> cis-Acon + H2O reversible isomerisation

Hydration cis-Acon + H2O / Aconitase -> Isocitrate I: FMN + FE S, II: FE S, III: b, FE S,
Oxidation Isocit + NAD+ / Isocit dehydro -> Oxalosucc + NADH + H + (NADH = 2.5 ATP)
Decarboxylation Oxalosucc / Isocit dehydro -> α-Keto + CO2 rate-limiting, irreversible stage, generates a 5C molecule c1, CYT C INBETWEEN 3/4: a, a3
Oxidative decarboxylation α-Keto + NAD+ + CoA-SH α-Keto dehydro, Thiamine PP, Lipoic acid, Mg++,transsuccinytase
Succinyl-CoA + NADH + H + + CO2 irreversible (NADH = 2.5 ATP), regenerates the 4C chain
substrate-level phosphorylation Succinyl-CoA + GDP + Pi Succinyl-CoA synthetase Succinate + CoA-SH + GTP
Oxidation Succinate + ubiquinone (Q) Succinate dehydrogenase Fumarate + ubiquinol (QH2)FADH2 to QH2 (Complex II) = 1.5 ATP
Hydration Fumarate + H2O Fumarase L-Malate Hydration of C-C double bond
Oxidation L-Malate + NAD+ Malate dehydrogenaseOxaloacetate + NADH + H+ reversible generates NADH (= 2.5 ATP)
NADH (-): pyruv dehydro, isocit dehydro, α-Keto dehydro, cit synth
AcCoA (-): pyruv dehydro,
succCoA (-): α-Keto dehydro
ATP (-) cit synth, α-Keto dehydro
Citrate (-) PFK
Ca (+): pyruv dehydro, isocit dehydro, α-Keto dehydro
CANCER: Carcinomas: cancer arising from epithelial cells, about 80% of cancers; Sarcomas: connective tissue or muscle cells; Leukemias: derived from leukocytes; lymphomas: derived from WBC precursors(hemopoietic cells); metastasis: development of secondary malignant growth; Ras proteins: monomeric
GTPases that help transmit signals from cell-surface receptors to the cell interior; p53 protein performs its job mainly by acting as a transcription regulator. Indeed, the most common mutations observed in p53 in human tumors are in its DNA-binding domain, where they cripple the ability of p53 to bind to its DNA target
sequences. Because p53 binds to DNA as a tetramer, a single mutant subunit within a tetrameric complex can be enough to block its function. The p53 protein exerts its inhibitory effects on the cell cycle, in part at least, by inducing the transcription of p21, which encodes a protein that binds to and inhibits the cyclin-
dependent kinase (Cdk) complexes required for progression through the cell cycle. Thus the p21 gene prevents the cell from progressing through S phase and replicating its DNA. The Apc protein, is an inhibitory component of the Wnt signaling pathway. It binds to the β-catenin protein, and helps to induce the protein’s
degradation. By inhibiting β-catenin in this way, Apc prevents the β-catenin from migrating to the nucleus, where it would act as a transcriptional regulator to drive cell proliferation and maintain the stem-cell state. SOME CARCINOGENS: VINYL CHLORIDE: liver angiosarcoma, BENZENE: acute leukemias ARSENIC:
skin carcinomas, bladder cancer ASBESTOS: mesothelioma RADIUM: osteosarcoma Desmosomes are a type of cell junction which connects two cells. Cadherin proteins link the adjacent cells together while Adaptor proteins link the junction to the intermediate filaments of either cell.

G1 (restriction):
pocket proteins (Rb - 1,2,3, p107 - 4,5, p130 - 4,5) bind 2 E2F to prevent cell cycle
progress
DNA damage/ growth factors -> cyclin D rises, binds to cdk4/6 -> inactivates Rb by
phosphorylation
D4/6 -> phosphorylates 107/130, E2F 4/5 are released -> cyclin E rises, binds to cdk2
E2 makes +feedloop, all or nothing switch, hyperphosphorylates rb -> E2F 1,2,3 frees ->
cyclin A/cdc 6 rise
cdk inhibitor 1b (p27) inhibits E/2, cyclin A rise blocks p27, which allows A to rise more
A/2 inhibits E2F 1-3 -> E2F 6-8 inhibit transcription
DNA damage/ any reason to halt in G1 -> ATM/ATR -> Chk1/2 -> cdc25A is degraded, E/2
is not activated
A/2 activates cdc 25, deactivates Wee1 -> activates B/1
as G2 progresses, Plk1 phosphors Wee1, degredation by SCF ubi ligase
cdc25/wee1 degrade -> cdc2 activate
Plk1+cdc25+cdc2 -> +feedloop to activate cdc2 and cyclin B rises

In a TIRF microscope, laser light shines onto cover-slip surface at critical angle at which total internal reflection occurs. Light does not enter sample, and the majority of
fluorescent molecules are not illuminated. However, electromagnetic energy does extend, as an evanescent field, for a very short distance beyond the surface of the cover
slip and into the specimen, allowing just molecules in the layer closest to the surface to become excited. When these molecules fluoresce, their emitted light is no longer
competing with out-of-focus light from the overlying molecules, and can now be detected. At present, the technique is restricted to a thin layer within only 100–200 nm of
the cell surface.
Oct4, Sox2, Klf4, and Myc, OSKM factors. When coexpressed, could reprogram mouse fibroblasts, permanently converting them into iPS cells; can continue dividing
indefinitely in culture, and become any differentiated cell, including functional germ cells. iPS cells can now be derived from adult human cells and from various other
differentiated cell types besides fibroblasts. As indicated, the master gene regulator proteins(OSK) induce both their own and each other's synthesis making a self-sustaining
feedback loop that helps to maintain cells in an embryonic stem cell-like state, even after all of the experimentally added OSKM initiators have been removed. Myc
overexpression speeds up early stages of the reprogramming process through the mechanisms shown. Myc overexpression enhances the efficiency of the process. Oct4
seems to have a central role and to be generally indispensable for the creation of iPS cells.