Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

D&T - E1 > Biochemistry > Flashcards

Biochemistry Flashcards

1
Q

DNA methylation at CpG islands results in

A

Repression of transcription

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Amino acids necessary for purine synthesis

A
  • Glycine
  • Aspartate
  • Glutamine

“GAG”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Drugs that disrupt pyrimidine synthesis

A
  • LEFLUNOMIDE (inhibits dihydroorate reductase)
  • METHOTREXATE, TRIMETHOPRIM, PYRIMETHANAMINE (inhibit dihydrofolate reducts which results in decreased dexoythymidine monophosphase [dTMP] in humans, bacteria, and protozoa, respectively)
  • 5-FLUOROURACIL (forms 5-F-dUMP, which inhibits thymidylate synthase and decreases dTMP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Drugs that disrupt purine synthesis

A
  • 6-MERCAPTOPURINE, AZATHIOPRINE (inhibit de novo purine synthesis)
  • MYCOPHENOLATE, RIBAVIRIN (inhibit inosine monophosphate dehydrogenase)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Drugs that disrupt purine and pyrimidine synthesis

A
  • HYDROXYUREA (inhibits ribonucleotide reductase)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Reaction catalyzed by HGPRT

A

Hypoxanthine + PRPP → IMP

Guanine + PRPP → GMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

DNA polymerase III

A
  • Prokaryotic only
  • Elongates leading strand by adding deoxynucleotides to the 3’ end
  • Elongates lagging strand until it reaches primer of preceding fragment
  • 3’→ 5’ exonuclease activty ‘PROOFREADS’ each added nucleotide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

DNA polymerase I

A
  • Prokaryotic only
  • Degrades RNA primer and replaces it with DNA
  • Has the same functions as DNA polymerase III but it also excises RNA primer with 5’→3’ exonuclease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

N-formylmethionine stimulates

A

Neutrophil chemotaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

RNA polymerase I

A

Makes rRNA (most numerous RNA, “r”ampant)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

RNA polymerase II

A

Make mRNA (largest RNA, “m”assive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

RNA polymerase III

A

Makes 5S rRNA, tRNA (smallest RNA, “t”iny)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Eukaryotic RNA polymerases

A
  • No proofreading function but can initiate chains

- RNA polymerase II opens DNA at promoter site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Prokaryotic RNA polymerase

A

1 RNA polymerase (multisubunit complex) makes all 3 kinds of RNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

α-amanitin

A
  • Found in Amanita phalloides (death cap mushrooms)
  • Inhibit RNA polymerase II
  • Causes severe hepatotoxicity if ingested
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Rifampin

A

Inhibits RNA polymerase in prokaryotes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Actinomycin D

A

Inhibits RNA polymerase in both prokaryotes and eukaryotes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Where does mRNA quality control occur

A

Cytoplasmic processing bodies (P bodies), which contain exonucleases, decapping enzymes, and miRNAs. mRNAs may be stored in P bodies for future translation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Where are miRNA genes located

A

In introns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

CDKs

A

Constitutive and inactive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Cyclins

A
  • Regulatory proteins that control cell cycle events
  • Phase specific
  • Activate CDKs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Cyclin-CDK complexes

A
  • Phosphorylate other proteins to coordinate cell cycle progression
  • Must be inactivated and inactivated at appropriate times for cell cycle to progress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Tumor suppressors

A
  • p53 induces p21, which inhibits CDKs → hypophosphorylation (activation) of Rb
  • Hypophosphorylation of Rb binds to and inactivates transcrption factor E2F → inhibition of G1-S progression
  • Mutations in these genes result in unrestrained cell division (eg Li-Fraumeni)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Permanent cells

A
  • Neurons, skeletal and cardiac muscle, RBCs

- Remain in G0 and regenerate from stem cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Stable (quiescent) cells

A
  • Hepatocytes, lymphocytes

- Enter G1 from G0 when stimulated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Labile cells

A
  • Bone marrow, gut epithelium, skin, hair follicles, germ cells
  • Never go to G0, divide rapidly with a short G1
  • Most affected by chemotherapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Nissl bodies

A
  • Rough endoplasmic reticulum in NEURONS

- Synthesize peptide neurotransmitters for secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Golgi protein modifications

A
  • Modifies N-oligosaccharides on aspargine (initially added onto protein in the RER)
  • Adds O-oligosaccharides on serine and threonine
  • Adds mannose-6-phosphate to proteins for trafficking to lysosomes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Enzyme defect in I-cell disease

A

N-acetylglucosaminyl-1-phosphotransferase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Signal recognition particle (SRP)

A
  • Abundant, cytosolic ribonucleoprotein that traffics proteins from the ribosome to the RER
  • Absent or dysfunctional SRP → proteins accumulate in the cytosol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

COPI

A
  • Golgi → golgi (retrograde)

- cis-Golgi → ER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

COPII

A

ER → cis-Golgi (anterograde)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Clathrin

A
  • trans-Golgi → lysosomes

- Plasma membrane → endosomes (receptor mediated endocytosis, eg LDL receptor activity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Microfilaments

A
  • Muscle contraction, cytokinesis

- Actin, microvilli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Intermediate filaments

A
  • Maintain cell structure

- Vimentin, desmin, cytokeratin, lamins, glial fibrillary acid proteins (GFAP), neurofilaments

36
Q

Microtubules

A
  • Movement, cell division

- Cilia, flagella, mitotic spindle, axonal trafficking, centrioles

37
Q

Vimentin stain

A
  • Mesenchymal tissue (eg fibroblasts, endothelial cells, macrophages)
  • Identifies mesenchymal tumors (eg sarcoma) but also many other tumors (eg endometrial carcinoma, renal cell carcinoma, and meningiomas)
38
Q

Desmin stain

A
  • Muscle

- Identifies muscle tumors (eg rhabdomyosarcoma)

39
Q

Cytokeratin stain

A
  • Epithelial cells

- Identifies epithelial cell tumors (eg squamous cell carcinoma)

40
Q

GFAP stain

A
  • Neuroglial cells (eg astrocytes, Schwann cells, oligodendrogia)
  • Identifies astrocytoma and glioblastoma
41
Q

Neurofilament stain

A
  • Neurons

- Identifies neuronal tumors (eg neuroblastoma)

42
Q

Drugs that act on microtubules

A
  • Mebendazole (antihelminthic)
  • Griseofulvin (antifungal)
  • Colchicine (antigout)
  • Vincristine/ Vinblastine (anticancer)
  • Paclitaxel (anticancer)

“Microtubules Get Constructed Very Poorly”

43
Q

Types of collagen

A
  • TYPE I → most common, Bone, Skin, Tendon, dentin, fascia, cornea, late wound repair
  • TYPE II → Cartilage (including hyaline), vitreous body, nucleus pulposus
  • TYPE III → Reticulin - skin, BLOOD VESSELS, uterus, fetal tissue, granulation tissue
  • TYPE IV → Basement membrane, basal lamina, lens

“Be So Totally Cool Read Books”
(bone, skin, tendon, cartilage, reticulin, basement membrane)

44
Q

Problems with formation of triple helix of collagen is associated with what disease

A

Osteogenesis imperfecta

45
Q

Problems with cross-linking of tropocollagen in the extracellular space is associated with which diseases

A
  • Ehlers-Danlos syndrome

- Menkes disease

46
Q

Describe the most common type of Ehlers-Danlos syndrome

A

Hypermobility type (joint instability)

47
Q

Describe the classical type of Ehlers-Danlos syndrome

A
  • Involves joint and skin symptoms

- Caused by a mutation in type V collagen

48
Q

Describe the vascular type of Ehlers-Danlos syndrome

A
  • Involves vascular and organ rupture

- Deficient type III collagen

49
Q

Menkes disease

A
  • X linked recessive connective tissue disease cause by impaired copper absorption and transport due to defective Menkes protein (ATP7A) [ATP7B is the gene implicated in Wilson’s disease]
  • Leads to ↓ activity of lysyl oxidase (copper is a necessary cofactor)
  • Results in brittle, kinky hair, growth retardation, and hypotonia
50
Q

How is Marfan syndrome related to elastin

A

Marfan syndrome is caused by a defect in fibrillin, a glycoprotein that forms a sheath around elastin

51
Q

What causes the wrinkles of aging

A

↓ collagen and elastin production

52
Q

How do collagen and elastin differ

A
  • Elastin is rich in NONhydroxylated proline, glycine and lysine residues
  • Tropoelastin has fibrillin scaffolding
53
Q

Southwestern blot

A

Identifies DNA-binding proteins (eg transcription factors) using labeled oligonucleotide probes

54
Q

Cre-lox system

A

Gene expression modification whereby one can inducible manipulate genes at specific developmental points (eg to study a gene whose deletion causes embryonic death)

55
Q

RNA interference

A

Gene expression modification whereby dsRNA is synthesized that is complementary to the mRNA sequence of interest. When transfected in human cells, dsRNA separates and promotes degradation of target mRNA, “knocking down” gene expression.

56
Q

Pleiotropy

A
  • One gene contributes to multiple phenotypic effects

- Example: untreated phenyketonuria (PKU) manifests with light skin, intellectual disability and musty body odor

57
Q

Dominant negative mutation

A
  • Exerts a dominant effect
  • A heterozygote produces a nonfunctional altered protein that also prevents the normal gene product from functioning
  • Example: mutation of a transcription factor in its allosteric binding site; nonfunctioning mutant can still bind DNA, preventing wild-type transcription factor from binding
58
Q

Hypophosphatemic rickets

A
  • X linked dominant
  • Formerly known as vitamin D resistant rickets
  • Inherited disorder resulting in ↑ phosphate wasting at proximal tubule
  • Results in rickets-like presentation
59
Q

Examples of X linked dominant disorders

A
  • Hypophosphatemic rickets
  • Rett syndrome
  • Fragile X syndrome
  • Alport syndrome
60
Q

Mitochondrial myopathies

A
  • Often present with myopathy, lactic acidosis, and CNS disease
  • MELAS syndrome (mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes)
  • Secondary to failure in OXPHOS
  • Muscle biopsy often shows “ragged red fibers”
61
Q

Cystic fibrosis pathophysiology

A
  • CFTR encodes an ATP-gated Cl- channel that secretes Cl- in lungs and GI tract and reabsorbs Cl- in sweat glands
  • MOST COMMON MUTATION: misfolded protein → protein retained in RER and not transported to cell membranes, causing ↓ Cl- (and H2O) secretion
  • ↑ intracellular Cl- results in compensatory ↑ Na+ reabsorption via epithelial Na+ channels → ↑ H2O reabsorption → abnormally thick mucus secreted into lungs and GI tract
  • ↑ Na+ reabsorption also causes more negative transepithelial potential difference
62
Q

Cystic fibrosis diagnosis

A
  • ↑ Cl- concentration in sweat (>60 mEq/L)
  • Can present contraction alkalosis and hypokalemia (ECF effects analogous to a patient taking a loop diuretic) because of ECF H2O/Na+ losses and concomitant renal K+/H+ wasting
  • ↑ immunoreactive trypsinogen (newborn screening)
63
Q

What is used as an anti-inflammatory agent in cystic fibrosis

A

Azithromycin

64
Q

X-linked recessive disorders

A
  • Ornithine transcarbamylase deficiency
  • Fabry disease
  • Wiskott-Aldrich syndrome
  • Ocular albinism
  • G6PD deficiency
  • Hunter syndrome
  • Bruton agammaglobulinemia
  • Hemophilia A and B
  • Lesch-Nyhan syndrome
  • Duchenne (and Becker) muscular dystrophy

“Oblivious Females Will Often Give Her Boys Her x-Linked Disorders”

65
Q

Causes of muscular dystrophies

A
  • Duchenne → frameshift, nonsense mutation, deletion
  • Becker → non-frameshift insertion or deletion
  • Myotonic type 1 → CTG expansion of DMPK gene (myotonin protein kinase)
66
Q

Most common cause of death from Duchenne muscular dystrophy

A

Dilated cardiomyopathy

67
Q

Function of dystrophin

A

Helps anchor skeletal muscle fibers, primarily in skeletal and cardiac muscle

68
Q

Lab findings for Duchenne muscular dystrophy

A
  • ↑ CK and aldolase

- Western blot and muscle biopsy confirm diagnosis

69
Q

Cause of Fragile X syndrome

A
  • X linked dominant inheritance

- Trinucleotide repeat in FMR1 gene (CGG) → METHYLATION → ↓ expression

70
Q

Heart condition found in Fragile X syndrome

A

Mitral valve prolapse

71
Q

Laboratory screens for trisomies

A

DOWN SYNDROME 1st TRIMESTER:

  • ↓ serum PAPP-A
  • ↑ free β-hCG

DOWN SYNDROME 2nd TRIMESTER:

  • ↓ α-fetoprotein
  • ↑ β-hCG
  • ↓ estriol
  • ↑ inhibin A

EDWARDS SYNDROME 1st TRIMESTER:

  • ↓ PAPP-A
  • ↓ β-hCG
  • ↓ α-fetoprotein
  • ↓ estriol
  • ↓ or normal inhibin A

PATAU SYNDROME 1st TRIMESTER:

  • ↓ β-hCG
  • ↓ PAPP-A
72
Q

3 ways to convert ethanol → acetaldehyde

A
  • CYTOSOL via alcohol dehydrogenase, generates NADH
  • MICROSOME via CYP2E1, consumes NADPH and generates ROS
  • PEROXISOME via catalase, generates H2O from H2O2
73
Q

Location of acetaldehyde dehydrogenase

A

Mitochondria

74
Q

Limiting reagent of alcohol metabolism

A

NAD+

75
Q

Ethanol metabolism ↑ NADH/NAD+ ratio in liver causes

A
  • Pyruvate → lactate (lactic acidosis)
  • Oxaloacetate → malate (prevent gluconeogenesis → fasting hypoglycemia)
  • Dihydroxyacetone phosphate → glycerol-3-phosphate (combines with fatty acids to make triglycerides → hepatosteatosis)
  • Disfavors TCA production of NADH
  • ↑ utilization of acetyl-CoA for ketogenesis (→ ketoacidosis) and lipogenesis (→ hepatosteatosis)
76
Q

Mitochondria is site for

A
  • Fatty acid oxidation (β oxidation)
  • Acetyl-CoA productino
  • TCA cycle
  • OXPHOS
  • Ketogenesis
77
Q

Cytoplasm is site for

A
  • Glycolysis
  • HMP shunt
  • Synthesis of steroids (SER)
  • Proteins (ribosomes, RER)
  • Fatty acids
  • Cholesterol
  • Nucleiotides
78
Q

Mitochondria and cytoplasm are both sites for

A
  • Heme synthesis
  • Urea cycle
  • Gluconeogenesis

“HUGs take 2”

79
Q

Kinase vs phosphorylase

A

Kinase catalyzes transfer of a phosphate group from a HIGH-ENERGY MOLECULE (usually ATP) to a substrate (eg phosphofructokinase)

Phosphorylase add inorganic phosphate onto substrate WITHOUT USING ATP (eg glycogen phosphorylase)

80
Q

Carboxylase

A

Transfers CO2 groups with the help of BIOTIN

81
Q

Mutase

A

Relocates a functional group within a molecule

82
Q

de novo synthesis of pyrimidine base production requires

A

Aspartate

83
Q

de novo synthesis of purine base production requires

A
  • Apartate
  • Glycine
  • Glutamine
  • THF
84
Q

Peroxisome

A
  • Membrane enclosed organelle involved in catabolism of very-long-chain fatty acids (through beta-oxidation), branched chain fatty acids, amino acid and ethanol
  • Refsum disease, Adrenoleukodystrophy – inability to metabolize long chain FAs
85
Q

Defects in the ubiquitin proteasome system have been implicated in some cases of

A

Parkinson disease

D&T - E1 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions