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Cellular Flashcards

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1
Q

CDKs

A

Regulation of cell cycle

Constitutive and inactive

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2
Q

Cyclin-CDK complexes

A

Phosphor late other proteins to coordinate cell cycle progression
Must be activated and inactivated at appropriate times for cell cycle to progress

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3
Q

Cyclin

A

Regulatory proteins that control cell cycle events
Phase specific
Activated CDKs

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4
Q

Tumor suppressors

A

p53 induces p21 which inhibits CDKs - hypo phosphorylation (activation) of Rb
Hypophosphorylated Rb binds to and inactivates transcription factor E2F - inhibition of G1-S progression
Mutations in these genes result in unrestrained cell division (e.g. Li-Fraumeni syndrome)

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5
Q

Cell types: permanent

A

Remain in G0
Regenerate from stem cells
Neurons, skeletal and cardiac muscle, RBCs

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6
Q

Cell types: Stable (quiescent)

A

Enter G1 from G0 when stimulated

Hepatocytes, lymphocytes

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7
Q

Cell types: Labile

A

Never go to G0, divide rapidly with a short G1
Most affected by chemotherapy
Bone marrow, gut epithelium, skin, hair follicles, germ cells

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8
Q

Rough Endoplasmic Reticulum (RER)

A

Site of synthesis of secretory (exported) proteins and of N-linked oligosaccharide addition to many provinces
Free ribosomes: unattached to any membrane site of synthesis of cytosolic and organellar proteins
Mucus-secreting goblet cells of the SI and Ab secreting plasma cells are rich in RER

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9
Q

Nissl Bodies

A

RER in neurons

Synthesize peptide neurotransmitters for secretion

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10
Q

Smooth Endoplasmic Reticulum (SER)

A

Site of steroid synthesis and detoxification of drugs and poisons
Lacks surface ribosomes
Liver hepatocytes and steroid hormone producing cells of the adrenal cortex and gonads are rich in RER

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11
Q

Cell cycle phases

A 
Checkpoints regulated by cyclin-dependent kinases (CDKs) and tumor suppressors 
M phase (shortest phase) includes mitosis (prophase, prometaphase, metaphase, anaphase and telophase) and cytokinesis (cytoplasm splits in two)
G1 and G0 are variable duration
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12
Q

Cell trafficking: Golgi

A

Golgi is the distribution center for proteins and lipids from the ER to the vesicles and plasma membrane
Modifies N-oligosaccharides on asparagine
Adds O-oligosaccharides on serine and threonine
Adds mannose-6-phosphate to proteins for trafficking to lysosomes

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13
Q

Cell trafficking: endosomes

A

Sorting centers for material from outside the cell or from the Golgi, sending it to lysosomes for destruction or back to the membrane/Golgi for further use

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14
Q

I-cell disease

A

Inclusion cell disease/mucolipidosis type II
Inherited lysosomal storage disorder with a defect in N-acetylglucosaminyl-1-phosphotransferase and failure of the Golgi to phosphorylate mannose residues on glycoproteins
Thus proteins are secreted extracellularly rather than delivered to lysosomes
results in coarse facial features, clouded corneas, restricted joint movement and high plasma levels of lysosomal enzymes
Often fatal in childhood

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15
Q

Signal Recognition Particle (SRP)

A

Abundant cytosolic ribonucleoproteins that traffics proteins from the ribosome to the RER
Absent or dysfunctional SRP - proteins accumulate in the cytosolic

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16
Q

Vesicular Trafficking Proteins

A

COP I: Golgi to Golgi (retrograde); cis-Golgi to ER
COP II: ER to cis-Golgi (anterograde)
Clathrin: trans-Golgi to lysosomes; plasma membrane to endosomes (receptor mediated endocytosis - LDL receptor activity)

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17
Q

Peroxisome

A

Membrane enclosed organelle involved in catabolism of very long chain fatty acids (beta oxidation), branched chain FAs, AAs and EtOH

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18
Q

Proteasome

A

Barrel-shaped protein complex that degrades damaged or ubiquitin-tagged proteins.
Defects in ubiquitin-protea some system have been implicated in some cases of Parkinson disease

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19
Q

Microfilaments

A

Function: muscle contraction; cytokinesis
Examples: actin, microvilli

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20
Q

Intermediate filaments

A

Function: maintain cell structure
Examples: vimentin, desmin, cytokeratin, lamins, glial fibrillary acid proteins, neurofilaments

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21
Q

Microtubules

A

Function: Movement, cell division
Examples: cilia, flagella, mitotic spindle, atonal trafficking, centrioles

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22
Q

Vimentin Stain

A

Cell type: mesenchymal tissue (fibroblasts, endothelial cells, MPs)
Identifies: mesenchymal tumors (sarcoma) but also other tumors (endometrial carcinoma, renal cell carcinoma, meningiomas)

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23
Q

Desmin Stain

A

Cell type: muscle

Identifies: muscle tumors (rhabdomyosarcoma)

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24
Q

Cytokeratin Stain

A

Cell type: epithelial cells

Identifies: epithelial tumors (squamous cell carcinoma)

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25
GFAP stain
Cell type: neuroglia (e.g. Astrocytes, Schwann cells, oligodendroglia) Identifies: astrocytoma, glioblastoma
26
Neurofilament Stain
Cell type: neurons | Identifies: neuronal tumors (e.g. Neuroblastoma)
27
Microfilament structure
Cylindrical outer structure composed of a helical array of polymerized heterodimers of alpha and beta Tubulidentata Each dimer has 2 GTP bound Incorporated into flagella, cilia, mitotic spindles (grows slowly and collapses quickly), also involved in slow axoplasmic transport in neurons
28
Molecular motor proteins
Transport cellular cargo toward opposite ends of Microtubule tracks Dynein- retrograde to microtubule (+ - -) Kinesin - anterograde to microtubule (- - +)
29
Drugs that act on Microtubules
``` Microtubules Get Constructed Very Poorly Mebendazole (anti-helminthic) Griseofulvin (antifungal) Colchicine (anti-gout) Vincristine/Vinblastine (chemotherapy) Paclitaxel (chemotherapy) ```
30
Cilia structure
9+2 arrangement of microtubule doublets The base of a cilium below the cell membrane, called the basal body, consists of 9 microtubule triplets with no central Microtubules
31
Axonemal dynein
ATPase that links peripheral 9 doublets and causes blinding of cilium by differential sliding of doublets
32
Kartagener Syndrome
Primary ciliary dyskinesia Immotile cilia due to a dynein arm defect Results in male and female infertility due to immotile sperm and dysfunctional Fallopian tube cilia Increased risk of ectopic pregnancy Can cause bronchiectasis, recurrent sinusitis, and situs in versus (e.d. Dextrocardia on CXR)
33
Plasma membrane composition
Asymmetric lipid bilayer Contains cholesterol, phospholipids, sphingolipids, glycolipids, and proteins Fungal membranes contain ergosterol
34
Na+/K+ pump
Na-K ATPase is located in the plasma membrane with ATP site on cytosolic side For each ATP consumed - 3Na+ go out of the cell and 2K+ enter the cell Ouabain inhibits by binding to K+ site Cardiac glycosides (digoxin) directly inhibit Na/K ATPase which lead to indirect inhibition of Na/Ca exchange increasing intracellular Ca and increasing cardiac contractility
35
Collagen
Most abundant protein in the human body Extensively modified by post-translational modification Organizes and strengthens extracellularly matrix
36
Type I collagen
Most common Bone (made by osteoblasts), skin, tendon, dentin, fascia, cornea, late wound repair Type I: Bone (decreased production in osteogenesis I perfecta type I)
37
Type II Collagen
Cartilage (including hyaline), vitreous body, nucleus pulposus Type II: CarTWOlage
38
Type III Collagen
Reticulin - skin, blood vessels, uterus, fetal tissue, granulation tissue Type III: deficient in the uncommon, vascular type of Ehlers-Danlos syndrome
39
Type IV Collagen
Basement membrane, basal lamins, lens Type IV: under the floor (BM) Defective in Alport syndrome; targeted by some autoAb in goodpasture syndrome
40
Collagen Synthesis (1)
Translation of collagen alpha chains (preprocollagen) Usually Gly-X-Y (proline-lysine) Glycine content best reflects collagen synthesis
41
Collagen Hydroxylation (2)
Hydroxylation of specific proline and lysine residues Requires VitC Deficiency = scurvy
42
Collagen Glycosylation (3)
Glycosylation of pro-alpha-chain hydroxylysine residues and formation of procollagen via hydrogen and DS bonds (triple helix of 3 collagen alpha chains) Problems forming triple helix - osteogenesis imperfect a
43
Collagen exocytosis (4)
Exocytosis of procollagen into extracellular space
44
Collagen Proteolytic processing (5)
Cleavage of disulfide rich terminal regions of procollagen --> insoluble tropocollagen
45
Collagen Cross Linking (6)
Reinforcement of many staggered tropocollagen molecules by covalent lysine-hydroxylysine cross linkage (by copper containing lysyl oxidase) to make collagen fibrils Problems with cross linking - Ehlers-Danlos syndrome, Menkes disease
46
Osteogenesis Imperfecta
Genetic bone disorder (brittle bone disease) caused by a variety of gene defects (most commonly COL1A1 and COL1A2) Most common form is the AD with decreased production of otherwise normal type I collagen Manifestations: multiple fractures with minimal trauma (may occur during birthing process), blue sclerae due to the translucent CT over choroid all veins, hearing loss (abnormal ossicles) Some forms have tooth abnormalities (opalescent teeth that wear easily due to lack of dentin)
47
Ehlers-Danlos Syndrome
Faulty collagen synthesis causing hyperextensible skin, tendency to bleed (easy bruising) and hypermobile joints Multiple types: inheritance and severity vary, can be AR or AD -Hypermobility type: joint instability, most common type -Classical type: joint and skin symptoms, caused by a mutation in type IV collagen -Vascular type: vascular and organ rupture, deficient type III collagen May be associated with joint dislocation, berry and aortic aneurysms, organ ruptures
48
Menkes Disease
X-linked recessive CT disease caused by impaired copper absorption and transport due to defective Menkes protein (ATP7A) Leads to decreased activity of lysyl oxidase (copper is a cofactor) resulting in brittle, kinky hair, growth retardation and hypotonia
49
Elastin
Stretchy protein within skin, lungs, large arteries, elastic ligaments, vocal cords, ligaments flava (connect vertebrae - relaxed and stretched conformations) Rich in no hydroxylases proline, glycine and lysine residues Tropoelastin with fibrillin scaffolding Cross-linking takes place extracellularly and gives elastin its elastic properties Broken down by elastase, which is normally inhibited by alpha-1 antitrypsin Wrinkles of aging are due to decreased collagen and elastin production
50
Marfan Syndrome
Caused by a defect in fibrillin (a glycoprotein) that forms a sheath around elastin
51
Emphysema
Can be caused by an alpha-1 antitrypsin deficiency resulting in excess elastase activity
52
Regulation by fructose-2,6-bisphosphate
FBPase-2 and PFK-2 are the same bifunctional enzyme whose function is reversed by phosphorylation by PKA Fasting state: increased glucagon - increased cAMP - increased PKA - increased FBPase-2, decreased PFK-2, less glycolysis and more gluconeogenesis Fed state: increased insulin - decreased cAMP - decreased PKA - decreased FBPase-2, increased PKA, more glycolysis and less gluconeogenesis
53
Pyruvate Dehydrogenase Complex
Mitochondrial enzyme complex linking glycolysis and TCA cycle. Differentially regulated in fed/fasted states (active in fed) Reaction: pyruvate + NAD+ + CoA -- acetyl-CoA + CO2 + NADH Complex (*TLC For Nancy*) Thiamine pyrophosphate (B1) Lipoic Acid CoA (B5, pantothenic acid) FAD (B2, riboflavin) NAD (B3, niacin) Activated by: increased NAD+/NADH ratio, ADP, Ca2+
54
Pyruvate dehydrogenase complex deficiency: findings
Causes a buildup of pyruvate that gets shunted to lactate (via LDH) and alanine (via ALT) - X-linked Neurologic defects, lactic acidosis, increased serum alanine starting in infancy
55
Pyruvate dehydrogenase complex deficiency: treatment
Increased intake of ketogenic nutrients (high fat content or increase lysine and leucine *Lysine and Leucine - the onLy pureLy ketogenic amino acids*
56
Pyruvate metabolism
Functions of different pyruvate metabolic pathways (and their associated co-factors) 1. Alanine aminotransferase (B6): alanine carries amino groups to the liver from muscle 2. Pyruvate carboxylase (biotin): oxaloacetate can replenish TCA cycle or be used in gluconeogenesis 3. Pyruvate dehydrogenase (B1, B2, B3, B5, lipoic acid): transition from glycolysis to the TCA cycle 4. Lactic acid dehydrogenase (B3): end of anaerobic glycolysis (major pathway in RBCs, WBCs, kidney medulla, lens, testes, and cornea)
57
TCA cycle (Krebs cycle)
The TCA cycle (in mitochondria) produces 3NADH, 1FADH2, 2CO2, 1GTP per acetyl-CoA = 10 ATP/acetyl-CoA (2x everything per glucose) Alpha-ketoglutarate dehydrogenase complex requires same cofactors as the pyruvate dehydrogenase complex (B1,B2,B3,B5, lipoic acid)
58
Substrates in TCA cycle
*Citrate Is Krebs' Starting Substrate For Making Oxaloacetate* (Acetyl-CoA + Oxaloacetate) -- citrate -- Isocitrate -- alpha-KG -- Succinyl-CoA -- Succinate -- Fumarate -- Malate -- Oxaloacetate
59
Electron Transport Chain and oxidative phosphorylation
NADH electrons from glycolysis enter mitochondria via the malate-aspartate or glycerol-3-phosphate shuttle FADH2 electrons are transferred to complex II (at lower energy level than NADH) The passage of electrons results in the formation of a proton gradient that, coupled to oxidative phosphorylation, drive the production of ATP
60
ATP produced by ATP synthase
1 NADH = 2.5 ATP | 1 FADH = 1.5 ATP
61
Electron Transport inhibitors
Directly inhibit ETC, causing a decrease in proton gradient and block of ATP synthesis * rotenONE: complex ONE inhibitor* * An-3-mycin (antimycin) A: complex 3 inhibitor* * CO/CN: complex 4 inhibitor (four letters)*
62
ATP synthase inhibitor
Directly inhibit mitochondrial ATP synthase, causing and increase in proton gradient. But not ATP is produced because ETC has stopped Oligomycin
63
Uncoupling Agents
Increased permeability of membrane, causing a decreased proton gradient and increased O2 consumption. ATP synthesis stops but ETC continues --> produces heat 2,4 Dinitrophenol (used illicitly for weight loss), aspirin (fever often occur after aspirin overdose), thermogenenin in brown fat
64
Gluconeogenesis: Pyruvate carboxylase
In mitochondria Pyruvate to Oxaloacetate Requires biotin, ATP, activated by acetyl-CoA
65
Gluconeogenesis: Phophoenolpyruvate carboxykinase
In cytosol Oxaloacetate to phosphoenolpyruvate Requires GTP
66
Gluconeogenesis: Fructose-1,6-bisphosphate
In ER Glucose-6-phosphate to fructose-6-phosphate Citrate (+), fructose 2,6 bisphosphate (-)
67
Gluconeogenesis: Glucose-6-phosphatase
In ER | Glucose-6-phosphate to glucose
68
Gluconeogenesis: facts
Occurs primarily in the liver serving to maintain euglycemia during fasting (also found in kidney, and intestinal epithelium) Deficiency in key gluconeogenic enzymes cause hypoglycemia (muscle cannot participate because it lacks glucose-6-phosphatase)
69
Odd-Chain FAs & TCA
Odd-chain FAs yield 1 propionyl-CoA during metabolism, which can enter the TCA cycle (succinyl-CoA), undergo gluconeogenesis, and serve as a glucose source Even chain FAs cannot produce a new glucose
70
HMP Shunt (pentode phosphate pathway)
Provides source of NADPH from abundantly available G6P -NADPH is required for reductive reactions, eg glutathione reduction inside RBCs, FA and cholesterol biosynthesis) Also provides ribose for nucleotide synthesis and glycolytic intermediates 2 distinct phases (oxidative & nonoxidative), both of which occur in the cytoplasm No ATP is used or produced
71
HMP shunt: Sites
``` (Sites of FA or steroid synthesis) Lactating mammary glands Liver Adrenal cortex RBCs ```
72
HMP: oxidative phase
Irreversible | G6P to CO2, 2 NADPH, Ribulose-5-phosphate via glucose-6-phosphate dehydrogenase
73
HMP: nonoxidative phase
Reversible Ribulose-5-phosphate to Ribose-5-P, Glyceraldehyde-3-phosphate and fructose-6-phosphate via phosphopentose isomerase, transketolases (requires B1)
74
Glucose-6-phosphate dehydrogenase deficiency
NADPH is necessary to keep glutathione reduced, which in turn detoxifies free radicals and peroxides Decreased NADPH in RBCs leads to hemolytic anemia due to poor RBC defense against oxidizing agents (eg fava beans, sulfonamides, primaquine, antituberculosis drugs) Infection (most common cause) can also precipitate hemolysis; inflammatory response produces free radicals that diffuse into RBCs causing oxidative damage
75
Glucose-6-phosphate dehydrogenase deficiency: Genetics
X-linked recessive disorder (most common human enzyme deficiency) More prevalent among African Americans Increased malarial resistance Findings: Heinz bodies - denatured Hemoglobin precipitates within RBCs due to oxidative stress, Bite cells - result from the phagocytic removal of Heinz bodies by splenic MPs
76
Essential fructosuria
Involves a defect in fructokinase (AR) Benign, asymptomatic condition since fructose is not trapped in the cell Symptoms: fructose appears in blood and urine
77
Fructose intolerance
Hereditary deficiency of aldolase B (AR) Fructose-1-phosphate accumulates causing a decrease in available phosphate which results in inhibition of glycogenolysis and gluconeogenesis Symptoms after consumption of fruit, juice or honey: hypoglycemia, jaundice, cirrhosis, vomiting Urine dipstick will be negative, reducing sugar can be detected in urine Tx: decrease intake of both fructose and sucrose (glucose+fructose)
78
Galactokinase deficiency
Hereditary deficiency of galactokinase (AR). Galactitol accumulates if galactose is present in diet Symptoms develop when infant begins to feed (lactose present in breast milk and routine formula): galactose in blood and urine, infantile cataracts May present as failure to track objects or to develop a social smile
79
Classic galactosemia
Absence of galactose-1-phosphate uridyltransferase (AR) Damage is caused by accumulation of toxic substances (including galactitol - esp in lens of eye) Symptoms: FTT, jaundice, hepatomegaly, infantile cataracts, intellectual disability, can lead to E. Coli sepsis in neonates Tx: exclude galactose and lactose (galactose+glucose) from diet *Fructose is to Aldolase B as Galactose is to UridylTransferase (FAB GUT)*

Biochemistry (6 decks)

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