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Biochemistry - Cellular

Terms in this set (56)

Cyclins
Regulatory proteins that control cell cycle events. Their concentration varies and is phase specific. They activate Cyclin Dependent Kinases(CDK).
Cyclin-CDK complexes
Phosphorylate other proteins and regulate cell cycle progression.
Cell cycle
- Interphase = G1 + S phase + G2
- G1: preparation for DNA replication + cell growth
- S phase: synthesis and replication of DNA
- G2: cell growth + DNA repair
Cell cycle checkpoints
- CDK inhibitors: p27, p21, p16
- From G1 to R point: cells respond to Mitogenic Growth Factors (GFs) and Tumour Growth Factor Beta (TGF-β) and other tumour Suppressor genes

Clinical note: In cancer, theses inhibitors are inactivated.
p53
Tumor Suppressor. It induces p21 that inhibits CDKs. It causes hypophosphorylation of the Rb protein, which causes it to remain bound to E2F and inactivates it. This inhibits the cell cycle at the G1 restriction point.
Tumor Suppressor genes
- Retinoblastoma (Rb)
- Tumour Growth Factor beta (TGF-β)
- p53
- Adenomatous polyposis coli (APC)
(picture indicates what type of cancer occurs if mutated)
Retinoblastoma protein (Rb)
It is an inhibitor of cell cycle progression from the G1 to the S phase of the cell cycle. It is active and bound to E2F. Cyclin-CDK Complex phosphorylates Rb and inactivates it. This releases E2F from Rb and the cycle proceeds from G1 phase, past R point, to the S phase.
Li-Fraumeni syndrome
Rare disorder that greatly increases the risk of developing several types of cancer, particularly in children and young adults. It is caused by a mutated p53 tumour suppressor gene.
Chromosomes
Packaged and organized structure containing most of the DNA. Are divided into two types: autosomes (body chromosomes) and allosomes (sex chromosomes). Humans have 23 pairs of chromosomes (22 pairs of autosomes and one pair of sex chromosomes), giving a total of 46 per cell.
Chromatid
Either of the two daughter strands of a replicated chromosome that are joined by a single centromere and separate during cell division to become individual chromosomes.
Mitosis
- Prophase: chromatin condenses into 2 chromosomes connected at the centimetre
- Prometaphase: nuclear membrane breaks apart
- Metaphase: chromosomes are dragged by microtubules and align in the equator of the cell
- Anaphase: chromosome breaks at the centomere and sister chromatids move to opposite ends of the cell
- Telophase: a set of chromatids (now called chromosomes) is present at each end of the cell and a nuclear membrane forms around each, producing two new nuclei.
Cytokinesis
Phase following telophase (mitosis) where the cytoplasm is divided in two.
"Permanent" cells
Neurone, skeletal and cardiac muscle, RBC: cells that remain in G0 phase (does not undergo replication). These cells regenerate only from stem cells.
"Stable" cells
Hepatocytes snd lymphocytes: cells that can enter G1 cell cycle phase, however only when stimulated.
"Labile" cells
Bonne marrow, gut epithelium, skin, hair and germ cells: cells that never go in G0 phase and divide rapidly with a short G1 phase.

Clinical note: they are most affected by chemotherapy.
Rough Endoplasmic Reticulum (RER)
Part of the endoplasmic reticulum to which ribosomes are attached: involved in the biosynthesis of proteins for export to the outside of the cell and enzymes to be incorporated into cellular organelles such as lysosomes.
Ribosome
Complex molecular machine that serves as the site of biological protein synthesis (translation). They link amino acids together in the order specified by mRNA molecules. Consist of two major components: the small ribosomal subunit (30S), which reads the RNA, and the large subunit (50S), which joins amino acids to form a polypeptide chain. Each subunit is composed of ribosomal RNA (rRNA) molecules.
Nissl bodies
Rough endoplasmic reticulum in neurons: organelle of the cell that synthesises peptide neurotransmitters.
Smooth Endosplasmic Reticulum (SER)
Sight of steroid synthesis and detoxification of drugs and poisons. Has NO surface ribosomes.

Clinical note: liver hepatocytes and hormone-producing cells in the adrenal cortex and gonads are rich in SER
Golgi Apparatus
It is the distribution center for proteins and lipids, transmitting these from the endoplasmic reticulum to vesicles (endosomes + lysosomes) and the plasma membrane. Acts by (phosphorylating) adding mannose-6-phosphate to proteins for trafficking to lysosomes.
Endosomes
Sorting centers for material from outside the cell or from the Golgi, sending this materials to lysosomes for destruction or back to the Golgi for further use.
Lysosomes
Vesicles that contain a variety of enzymes in order to be able to break down the variety of biomolecules engulfed by the cell (peptides, nucleic acids, carbohydrates, and lipids). The enzymes responsible for this hydrolysis require an acidic environment for optimal activity. Also capable of fusing with other organelles & digesting large structures or cellular debris. They are able to conduct autophagy, clearing out damaged structures. Similarly, they are able to break-down virus particles or bacteria in phagocytosis of macrophages.
I-cell disease
Inherited lysosomal storage disorder caused by a defect in N-acetylglucosaminyl-1-phosphotransferase. This leads to a failure of the Golgi to phosphorylate mannose residues on glycoproteins causing proteins to be secreted extracellulary rather than transferred to lysosomes.

Symptoms: coarse facial features, clouded corneas, restricted joint movement, high plasma levels of lysosomal enzymes.
Signal Recognition Particle (SRP)
Ribonucleoprotein responsible for trafficking proteins from the ribosome to the RER.

Clinical note: if absent or dysfunctional, proteins will accumulate in the cytosol.
Peroxisome
Membrane-enclosed organelle that catalises (via β-oxydation) very-long-chain fatty acids, amino acids and ethanol.
Proteasome
Barrel-shaped protein complex that degrades damaged or ubiquitin-tagged proteins.
Clinical note: a defect in the ubiquitin-proteasome system might cause Parkinson's disease
Cytoskeleton
Network of protein fibres within the cytoplasm that supports cell structure + cell and organelle movement + cell division
Microfilaments
Actin and Microvilli: responsible for muscle contraction and cytokinesis
Intermediate filaments
Vimentin, Desmin, Cytokeratin, Lamins, Neurofilaments and Glial Fibrillary Acid Proteins (GFAP): maintain cell structure
Microtubules
Cilia, Flagella, Mitotic spindle, Axonal trafficking and Centrioles: responsible for movement and cell division. They have a cylindrical outer structure composed of a helical array of polymerised heterodimers of alpha- and beta- tubulin.
Vimentin
Intermediate filament found in mesenchymal tissue: fibroblasts, endothelial cells and macrophages
Desmin
Intermediate filament found in muscle
Cytokeratin
Intermediate filament found in epithelial cells
Glial Fibrillary Acid Proteins (GFAP)
Intermediate filament found in neuroglial cells: astrocytes, Schwann cells and oligodendroglia
Dynein
Molecular motor protein that transports cellular cargo retrograde to the microtubule
Kinesin
Molecular motor protein that transports cellular cargo anterograde to the microtubule
Mebendazole
Anthelminthic drug (destroy parasitic intestinal worms) that acts on microtubules
Griseofulvin
Antifungal drug that acts on microtubules
Colchicine
Antigout drug that acts on microtubules
Vincristine and Vinblastine
Anticancer drugs that act on microtubules
Paclitaxel
Anticancer drug that acts on microtubules
Cilia
Microtubule organelle made of 9 peripheral and 2 central microtubule doublets.
Note: Axonemal dynein is the ATpase that links the 9 peripheral doublets and causes bending of cilium by differential sliding of these doublets.
Kartagener syndrome
Also called primary ciliary dyskinesia: immotile cilia due to dyne arm defect. Results in male and female infertility due to immotile sperm and dysfunctional fallopian tube cilia; respectively. This increases the risk of ectopic pregnancy. Can cause recurrent sinusitis, bronchiectasis and situs inversus (dextocardia!)
Plasma membrane
Asymmetric lipid bilayer that contains cholesterol, phospholipids, sphingolipids, glycolipids and proteins.
Sodium-Potassium pump (Na+/K+ ATPase)
Located on the plasma membrane, this pump has its ATP site on cytosolic side. For each ATP consumed, 3Na+ go out of the cell and 2K+ come into the cell.

Clinical note: Ouabain inhibits this pump by binding to the K+ site.
Ouabain
Poison that inhibits the Na+/K+ ATPase by binding to the K+ site. Leads to an increase in intracellular Na+, which activates the Na+/Ca2+ exchanger and ultimately increases Ca2+ inflow.
Digoxin and Digitoxin
Cardiac glycosides: inhibit the Na+/K+ ATPase which leads to an increase in intracellular Na+, which activates the Na+/Ca2+ exchanger and ultimately increases Ca2+ inflow; leading to a positive inotropic effect on cardiac myocytes.
Collagen
Most abundant protein of body: organises and strengthens extracellular matrix.
(Pneumonic): Be So Totally Cool, Read Books.
B: Bone (Type 1)
S: Skin (Type 1)
T: Tendon (Type 1)
C: Cartilage (Type 2)
R: Reticulin (Type 3)
B: Basement membrane (Type 4)
Type 1 collagen
Most common type (90%) of collagen, found in bone (osteoblasts), skin, tendons, fascia, dentin, the cornea and late wound repair.

Clinical note: decreased production in osteogenesis imperfect type 1
Type 2 collagen
Collagen found in cartilage (hyaline) and the vitreous body.
Type 3 collagen
Collagen found in reticulin (skin), blood vessels, uterus, fatal tissue and granulation tissue.

Clinical note: deficient in a rare vascular type of Ehlers-Dalos Syndrome (ThreE -> Dalos)
Type 4 collagen
Collagen found in the basement membrane, basal lamina and lens.

Clinical note: defective in Alport Syndrome and targeted by autoantibodies in Goodpasture Syndrome.
Collagen synthesis
Osteogenesis imperfecta (Brittle bone disease)
Autosomal dominant genetic bone disorder caused by a variety of gene defects (COL1A1 and COL1A2). Leads to a decreased production of type 1 collagen.
Symptoms: multiple fractures + fractures during birth + blue sclerae (white area around the pupil) + gearing loss caused by abnormal ossicles + tooth abnormalities (lack of dentin)
Ehlers-Danlos Syndrome
Condition where faulty collagen synthesis causes hyper extensible skin, hyper mobile joints and can leads to bleeding and aneurysms.
- Hypermobility type: most common
- Classical type: caused by a mutation in type 5 collagen
- Vascular type: caused by a deficient type 3 collagen
Menkes disease
X-linked recessive connective tissue disease caused by impaired COPPER absorption and transport due to defective Menkes protein (ATP7A). Leads to a decrease in activity of lysol oxidase.

Symptoms: brittle hair, growth retardation and hypotonia.
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