MCM Review

Question 1

What is the only source of pluripotent stem cells?

Answer 1

Cells of the inner cell mass

Question 2

What is the problem in methemoglobin?

Answer 2

Iron is in its ferric state (Fe3+) and will not bind oxygen

Question 3

Differentiate direct vs indirect methemoglobin

Answer 3

Direct –> genetically linked

Indirect –> oxidation by other compounds

Question 4

What kind of shift does methemoglobin cause?

Answer 4

Left shift of oxygen curve

Question 5

What kind of shift does anemia induce?

Answer 5

Anemia causes a right shift of the oxygen curve (decreased affinity

Question 6

A patient has a blood oxygen content of 17.25 mL/dL and a hemoglobin concentration of 15.1 g/dL. The patient’s oxygen saturation is best described as which of the following?
A. Normal oxygen saturation (97-99%)
B. Decreased oxygen saturation (<97%)
C. Maximum oxygen saturation (100%)

Answer 6

B Decreased oxygen saturation (<97%)

1.34 mLO2/1gHb x 15.1g/dL

Question 7

How many mL of oxygen are there per gram of hemoglobin?

Answer 7

1.34 mL O2/1 gHb

Question 8

What clinical situations could indicate a left shift of oxygen to blood?

Answer 8

Polycythemia

Methemoglobemnia

Question 9

What is primary polycythemia (Vera)

Answer 9

⬇️ EPO

Extra RBCs

⬆️ blood volume x2

⬆️ viscosity

normal CO

Question 10

Why are silent mutations not harmful?

Answer 10

First two letters of codon often the same, but the third is able to be 3 separate codons so the same amino acid product is still possible

Question 11

What mutations of DNA can be significantly detrimental?

Answer 11

Nonsense and frameshift mutations

Question 12

What causes Sickle cell anemia?

Answer 12

Single base substitution of Glu for a Val (hydrophobic, neutral)

Question 13

What common energy expenditure is constant for all three steps of mRNA translation?

Answer 13

All three steps utilize GTP

Question 14

What are the prokaryotic elongation inhibitors?

Answer 14

Tetracycline –> binds 30S, blocks tRNA entry

Chloramphenicol –> inhibits peptidyl transferase

Clindamycin/erythromycin –> binds 50s, blocks ribosomal translocation

Question 15

What are the eukaryotic elongation inhibitors?

Answer 15

Cycloheximide –> inhibits peptidyl transferase

Diptheria Toxin –> inactivates GTP-eEF2

Shiga Toxin/Ricin –> binds 60s, blocks tRNA entry

Question 16

What is the role of puromycin?

Answer 16

A eukaryotic elongation inhibitor that shares a similar structure to tyrosyl-tRNA

Enters A site and causes premature stop

Question 17

What do initiation factors attached to small ribosomal subunit do?

What do initiation factors attached to met-tRNA do?

Answer 17

Small ribosomal subunit –> promotes binding of codon and anticodon of tRNA

IF attached to met-tRNA –> hydrolyzes GTP to provide energy for formation of initiation complex

Question 18

Where are proteins destined that are made in the cytoplasmic pathway?

Answer 18

Cytoplasm

Mitochondria

Nucleus

Question 19

What is the nuclear translocation signal?

Answer 19

KKKRK (tryptophan rich signal)

Question 20

What is the mitochondrial translocation signal

Answer 20

An N-terminal hydrophobic α- helix peptide

Question 21

What residues does O-glycosylation target?

Answer 21

Ser and Threonine

Question 22

What does N-guyscosylation target?

Answer 22

Asn and Gln

Question 23

What residues does phosphorylation target?

Answer 23

Ser, Tyr, Asp, Thr, His

Hydroxyls (OH)

Question 24

What residue does disulfide bonding target?

Answer 24

Cystine residues

Question 25

What may happen if a diabetic has an over-abundance of glycosylation?

Answer 25

Cataract formation in the eye

Question 26

What happens in Alzheimer's Disease?

Answer 26

A mutated gene that produces amyloid precursor protein (APP) formation of neurotic plaques Supplementation with lys may

Question 27

What happens in Mad Cow disease?

Answer 27

Introduction of prions (misfolded proteins) that induce the same formation in their counterparts

Question 28

What happens in Huntington's Disease?

Answer 28

Protein aggregations in the brain CAG repeats = polyglutamine (polyQ) tract The abnormal Huntington protein (mHTT) forms intramolecular hydrogen bonds and aggregates

Question 29

What happens in Parkinson's disease?

Answer 29

Mutated α-synuclein results in aggregates that form Lewy bodies Function form is an α-helix while the febrile form is β-sheet Results in neuronal death of the midbrain and a lack of available dopamine

Question 30

Describe endocrine signaling?

Answer 30

Long distance Signaling - hormone

Question 31

Describe paracrine signaling?

Answer 31

Signal diffused to neighboring cell - NMJ

Question 32

Describe autocrine signaling?

Answer 32

Signaling cell is the targeting cell

Question 33

Where do hydrophobic signal target?

Answer 33

The nucleus

Question 34

Where do small polar hydrophilic signals target?

Answer 34

An EC receptor that utilizes secondary messengers

Question 35

What are some sensory input for GPCRs?

Answer 35

Photons, ions, amino acids

Question 36

An active GPCR switches out ________ for ______ via ________

Answer 36

GDP, GTP, GEF

Question 37

What is the role of Gαs?

Answer 37

Stimulates production of cAMP via adenylate cyclase ultimately activating PkA

Question 38

What is the role of Gαi

Answer 38

Inactivates adenylate cyclase = no PKA

Question 39

What is the role of Gαq

Answer 39

Activates PLC (phospholipase C) causing the cleavage of PIP2 --> IP3 & DAG (ca2+ also)

Question 40

What is the role of G protein receptor kinases? What is the end goal?

Answer 40

End goal - to desensitize the G protein GRK phosphorylates GPCRs to which Arrestin can bind (3rd IC loop) and inhibit

Question 41

What's happening in cholera?

Answer 41

Gαs is constantly active. The resulting cAMP keeps Cl- channels constantly open

Question 42

What's happening in Pertussis?

Answer 42

Gαi is inhibited, excessive cAMP produced via adenylate cyclase Dried out airways

Question 43

What pathways are activated by RTK signaling?

Answer 43

Ras - dependent Ras - independent

Question 44

What blotting technique allows for visualizing of protein?

Answer 44

Western blot

Question 45

What blotting technique visualizes DNA?

Answer 45

Southern blotting

Question 46

What blotting technique visualizes RNA?

Answer 46

Northern blot

Question 47

What is the problem with the heat-stable DNA polymerase used in PCR?

Answer 47

It has no proofreading capability an is described as a "dirty" method

Question 48

What is RFLP used for?

Answer 48

Forensics

Question 49

What is VNTR (variable number of tandem repeats)

Answer 49

Diagnostics of disease (Huntington's)

Question 50

What is one use of recombinant gene technology?

Answer 50

Insulin production (better than wild type)

Question 51

What is the use of ELISA?

Answer 51

Practical use --> HIV ag

Question 52

What's the difference between indirect and sandwich ELISA?

Answer 52

Indirect --> Target is Ag Sandwich --> target is Ab

Question 53

What is the only version of totipotency?

Answer 53

Zygote

Question 54

What are the examples of pluripotency?

Answer 54

1. ) ICM of a blastocyst | 2. ) iPS

Question 55

What can be associated with embryonic stem cells?

Answer 55

Teratomas, cancer, unrestricted growth

Question 56

What growth factors produce an adipocyte?

Answer 56

Retinoic acid + insulin + thyroid hormone

Question 57

What growth factors produce a neuron?

Answer 57

Retinoic acid

Question 58

What potency is cord blood?

Answer 58

Multipotent

Question 59

What potency are fetal stem cells?

Answer 59

Multipotent

Question 60

What potency are hematopoietic stems cells?

Answer 60

Multipotent

Question 61

What change in potency does iPS induce?

Answer 61

Taking a somatic multipotent cell and changing into a pluripotent cell

Question 62

What are 5 important growth factors needed to induce iPS?

Answer 62

Oct 3/4, Sox-2, Myc (n-Myc and c-Myc), Nanog, FoxD3

Question 63

Does urobilinogen have color?

Answer 63

No, it's translucent

Question 64

Discern PKU from Cystic Fibrosis

Answer 64

Multiple genotype, one phenotype - Cystic Fibrosis One genotype, multiple phenotypes - PKU

Question 65

What does chemotaxis use to change

Answer 65

Monomeric G protein --> pip3 --> Ras --> ARP --> Rho

Question 66

What is the consequence of an intra-hepatic jaundice

Answer 66

Build-up in the blood of conjugated and unconjugated billirubin Increase in ALT and AST

Question 67

What's the consequence of post-hepatic jaundice

Answer 67

Elevated blood levels of conjugated billirubin

Question 68

Break down of heme, what is the first enzyme to act on heme? (Rate-limiting step before the liver)

Answer 68

Heme oxygenase

Question 69

What type of signaling is Talin and FAK?

Answer 69

Talin (in --> out) | FAK (out --> in)

Question 70

What is a good thing to know about FAK?

Answer 70

It's a drug target

Question 71

What happens in secondary polycythemia?

Answer 71

Abnormal CO ⬆️ EPO ⬆️ RBCS

Question 72

What changes in Physiologic polycythemia?

Answer 72

Normal CO ⬆️ RBCs ⬆️ EPO

Question 73

What does activation of the RAS-dependent pathway lead to?

Answer 73

Gene transcription (increased glucokinase transcription)

Question 74

What does the activation of the RAS-independent pathway lead to?

Answer 74

Alteration of protein and enzyme activity - GLUT 4 sequestering activation of glycogen synthase

Question 75

What are important growth factors found in pluripotent cells?

Answer 75

Cripto and GDF-3

Question 76

What two diseases are related to intra-hepatic jaundice?

Answer 76

Criggler-Najjar syndrome Gilbert syndrome

Question 77

What are all the cyclin-Cdks and what phases do they operate in?

Answer 77

Cyclin - D | D | E | A | A | B Cdks - 6 | 4 | 4 | 2 | 2 | 1 Phase -G1|G1| S | S |G2|G2

Question 78

Discern Prader Willi Syndrome from Angelman Syndrome

Answer 78

Prader Willi - paternal chromosome deletion (maternal silenced) Angelman Syndrome - maternal chromosome deletion (paternal silenced)