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Biology > Review Session Terms I should Know > Flashcards

Review Session Terms I should Know Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

Adheren Junction (what is made it made of)

A

cell-cell (homophilic) and cell-ECM interactions (heterophillic)
actin-actin interaction and actin-intermediate filament interaction

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2
Q

Desmosome (what is made it made of)

A

cadherin, desmoplakin linker protein, and intermediate filament

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3
Q

Hemidesmosome (what is made it made of)

A
  • integrin a6/b4, desmoplakin like protein, and intermediate filament
  • binds to the ECM
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4
Q

Pemiphagus

A

autoimmune attacking on your caderhins

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5
Q

Ehlar Danlos Syndrome

A

mess up (defect) in keratin intermediate filament assembly (stretchy skin)

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6
Q

Type IV collagen

A

-type of collagen forms a meshwork in basal lamina (can not form fibrils)

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7
Q

Basal Laminin

A
  • made of Type IV collagen, lamilln, and proteoglycan

- function in muscle, kidney filter, and regulates cell proliferation

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8
Q

what are the mechanisms of converting proto-oncogene to oncogene?

A
  • point mutations
  • gene amplification
  • chromosomal rearrangement
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9
Q

DNA Viruses can cause cancer by

A

expressing genes in their genome that block action of Rb and p53

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10
Q

Malignant cancer (invasive) are a result of

A

a series of mutations (ie. LOF of p53 and mutation of Ras that makes it overactive)

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11
Q

Steroid for some genes act as

A

partner transcription factors to activate gene expression

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12
Q

CAM kinases are aka

A

calmodulin (ie. Myosin light chain Kinase)

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13
Q

JAK-STAT is

A

is a type of Receptor tyrosine but lacks the kinase activity (no transphorylation)

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14
Q

cyclin subunit is turned off during the end of mitosis by

A

ubiquitination via E3 ligase

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15
Q

cyclin +regulatory unit=

A

complete cyclin-dependent Kinase (cdk)

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16
Q

once cyclin was binds to regulatory unit your have inhibitory and activating kinase called

A

wee1 and activating kinase(cak)

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17
Q

For a resistant virus to to proliferate in patient the HIV protease should have

A

both a higher Ki than the wild type (can’t bind the inhibitor well) and kcat/km near wild-type level (can process polyprotein)

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18
Q

2 ways in which you can have HIV drug failure is.. what is the solution?

A

Patient may clear drug too rapidly
Patient has poor compliance

-solution is to change to different drugs that can help (hopefully some that can reduce ADRs and also fight virus)

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19
Q

One big difference between HIV and HCV in why HIV persists in your body while though expensive in treatment HCV can be completely cleared from your body is…

A

HIV can integrate into your genome, HCV doesn’t.

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20
Q

Dendritic cells

A
  • APCs
  • activate naive T cells
  • FDCs provide aid in the maturity of B cells providing cytokines during during its migration to the periphery
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21
Q

Importance differences BCR and TCR

A
  • TCR aren’t secreted

- TCR doesn’t undergo somatic hypermutation

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22
Q

What are super-antigens?

A

bacterial proteins that link the MHC molecule and TCR (variable B genes of it) together. Stimulating substantial cytokine signaling than the conventional Ag.

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23
Q

What is an important reaction needed between the Tcell and target (B cells, APC [DC])

A
  • CD40 (on the Tcell target)-CD40L (on Tcell)
  • B7-CD28
  • TCR-Ag-MHC
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24
Q

Heterotaxy

A
  • Solitus ambiguous

- mix in normal and abormal laterality (due to morphogen on both sides of embryo

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25
Q

During Implantation

A

-trophoblast cells attach to the wall of the endometrium (uterine lining)

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26
Q

Spina bifida (surgical repairable) or anenchephaly (fatal) occurs due to defect in

A

neural plate closure

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27
Q

Birth Defects are most sensitive at weeks

A

3-8

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28
Q

Birth defects can be induced by

A

Environment (alcohol and drugs, viruses) and pharmacologic products and genetics.

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29
Q

asymmetric flow is able to move from right to left axis due to morphogen flow via

A

ciliated epithelium (pushed by calcium release)

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30
Q

Epidermolysis Bullosa

A

inability to synthesize intermediate filaments like desmosomes and hemi-desmosomes (blistered skin)

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31
Q

laminin does what?

A
  • cross-linker protein
  • apart of Basal lamina
  • aids in wound healing and clots
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32
Q

Fibroconnectin

A
  • cross linker proteins

- apart of basal lamina

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33
Q

Mechanisms of Enzyme Regulation

A

1) Allosteric regulation
2) Reversible modification
3) Irreversible Modification
4) Protein-Protein interactions

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34
Q

Allosteric regulation and an example

A

modulator binds at site away from active site, affecting its activity

ie. ATcase with ATP increasing its activity (activator of the R state) and CTP decreasing its acitvity (inhibitor which favors the T state

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35
Q

Reversible Modification

A

alter enzyme by causing conformational change that affects catalysis (conformation) or altering cellular localization of enzyme

ie. phosphorylation via kinase is a important one

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36
Q

Irreversible modification

A

covalent modification
ie. Zymogen are synthesized (inactive form) and are activated irreversibly at the time and place where they are needed, clotting cascade (factor proteins are serine proteases)

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37
Q

Regulation of Protein-Protein Interactions

A

ie. Anti-Thrombin, Pancreatic Anti-tryspin, and alpha 1-anti-trypsin

zymogen activation though irreversible, can interact with inhibitor proteins (plasmin), calmodulin binding interactions with other proteins via Ca2+ binding.

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38
Q

Clotting protein via this enzyme causes the clotting protein to form with gamma carboxy glutamate, allowing binding to the phospholipid….

What drugs inhibit this enzyme

A

Vitamin K dependent Protein

Anti-coagulants (ie. Warfarin)- slowing clotting

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39
Q

After rapid clotting formation, localization to the site of injury, you then get rapid termination via..

A

plasminogen conversion to plasmin. Plasmin is a reversible inhibitor or zymogen activation which acts to hydrolyze and remove the fibrin clot.

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40
Q

The best protease inhibitors mimic the ..

A

the transition state conformation

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41
Q

Anti-thrombin (ATIII), what does it do and what happens if you don’t have this protein?

A

inhibitor protein that stops clotting by inactivating the serine proteases and thrombin

-without it you will have thrombosis (formation of too many clots which isnt good)

42
Q

alpha 1 Anti-trypsin (AT-I), what does it do, without it what would happen?

A
  • inhibits elastase in the lung

- without it you would have very little elastin in the lungs, causing emphysema like symptoms (ie. SOB)

43
Q

Pancreatic Trypsin Inhibitor

A

Inactivates inappropriate activation of proteases in the pancreaas

44
Q

T cell receptors that are MHC Restricted means

A

they have to interact with the right MHC molecule on the B cell and APC and the MHC has to have the antigen, and the TCR has to recognize both for T cell to activate

45
Q

the complement receptors that aids in B cell binding to the Ag to find it is…

A

CD3 and CD19

46
Q

transmembrane IgM and IgD to secreted IgM and IgD are made via which splicing..

A

RNA splicing

47
Q

secreted IgG isotypes are made via which splicing..

A

DNA splicing

48
Q

Both IgM, IgD, and IgG splicing are activated via

A

AID

49
Q

Remember that cancer can be expressed when

A

-you have multiple genes (proto-oncogenes and tumor suppressors) mutated

50
Q

CML is

A

is a proto-oncogene that is gives you leukemia when you have chromosomal translocation t(9:22)

51
Q

Chromosome Breakage Syndromes

A

disorders associated with defect in DNA repair mechanisms or genomic instability, and patients with these disorders show increased predisposition to cancer.

ie. HNPCC (mismatch repair defect)

52
Q

Protooncogenes

A
  • genes that are involved with cell proliferation
  • are dominantly acting
  • result in leukemias and lymphomas
  • mutations are usually translocations (chromosomal rearrangements), gene amplifications, and pt. mutations (less common)
  • mutations are acquired
  • usually becomes an oncogene due to gain and change of function
53
Q

Tumor suppressor

A
  • genes which are involved in cell growth control
  • They are recessive acting
  • mutations inherited
  • mutations cause solid tumors
54
Q

Types of Prenatal Testing, which one is ideal to do?

A

Non-invasive and Invasive. Preference is for non-invasive

55
Q

Ultrasound (what is it, advantages and disadvantages, what do you find?)

A
  • around 18 weeks gestation
  • verifies viability, possible abnormalities and a variety of defects (ie. Down Syndrome, Clefting)
  • Determines gestational age, and multiple pregnancies.
56
Q

NIPS testing (what is it, advantages and disadvantages, what do you find?)

A
  • uses cell free dna from maternal blood giving information of the fetus as well.
  • isolated 10-22 weeks gestation

Two methods:

Counting method- detects aneuploidies (ie. trisomy) but can not differentiate between maternal and fetal abnormalities, and a vanishing twin.

SNP based NIPS- detects aneuploidies more accurately and can differentiate between mother and fetal abnormalities, and vanishing twin.

57
Q

MSAFP testing

A

-non-invasive blood test
- gestational age of 15-20 weeks
- screening test for risk assessment of fetus
High levels- ONTD
Low levels- Down syndrome
-Disadvantages: less sensitive and does not predict outcome (remember just risk)

58
Q

AFAFP testing (what is it, advantages and disadvantages, what do you find?)

A
  • runs AFP on the amniotic fluid extracted from the amniocentesis procedure.
  • low AFP levels (confirmed with Karyotype analysis and FISH) indicate risk of:
  • trisomies 13, 18, and 21
  • triploidy
  • Mosaic turner syndrome

high AFP levels indicate:

open neural tube defects (ONTD) - is confirmed via acetylcholinesterase test.

59
Q

Chorionic Villus Sampling (what is it, how many weeks gestation, advantages and disadvantages, what do you find?)

A
  • Invasive
  • 10-14 weeks gestation
  • advantage: can be done earlier
  • Disadvantage: higher risk of limb reduction if before 10 weeks and higher risk than amniocentesis of abortion 1/100
60
Q

Amniocentesis (what is it, how many weeks gestation)

A
  • Invasive
  • 16-18 weeks gestation
  • removes some aminotic fluid which contains some fetal cells which can be used to do multiple tests

disadvantages
-there is some risk 1/300 result in abortion

61
Q

Mitochondrial diseases are inheritance patterns are

A

autosomal and x-linked mutations of nuclear genes or chromosome itself.

62
Q

Forensic DNA analysis strategies

A

Mitochondrial DNA analysis and Nuclear DNA Analysis

63
Q

Mitochondrial DNA analysis

A

-creates family identity linked through the mom and her siblings (which have the same mitochondria

64
Q

Nuclear DNA analysis

A

(preferred for unique identification)

  • Involves DNA Fingerprinting and micro satellite analysis
  • used alot in criminical inclusions and exclusions of suspects, and paternity and testing
  • differentiates between siblings
65
Q

Personalized medicine

A
  • genotype is found in the individual and used for preventative treatment before disease shows symptoms.
    (ie. Angelina Jolie finding out she has BRCA mutation and cutting her breasts off as a result of that, prior to getting the disease..it helped her knowing)
66
Q

PGD (Pre-implantation Genetic Diagnosis)

A

-screens the baby at the embryo stage, by removing the cell and undergoing FISH to see for abnormality

67
Q

Next Generation Sequencing (Assisted Diagnostic Technology)

A
  • used to sequence the whole genome of fetus

- will eventually replace PGD

68
Q

Types of Screening testing in Pregnancy

A

Carrier, Newborn, and Prenatal Testing

69
Q

Carrier Testing

A

risk assessment of being a carrier before the baby is born

70
Q

Newborn Testing

A

-testing for disorder of the baby already born

71
Q

Prenatal Testing

A

-testing for likelihood of disorder in the fetus

72
Q

RSV (the basics)

A
  • enveloped virus that infects infants at the respiratory epithelium, causing croup
  • leaves the cell via budding
73
Q

CMV

A
  • virus cause Mono-like symptoms but different than EBV that it doesn’t produce sore throat
  • can cause systemic disease in immunocompromised
  • causes rash, jaundice, hepatosplenomalgy
74
Q

What are the risk factors for Breast cancer?

A
  • advanced age
  • family history
  • BRCA gene mutations
  • Ethnicity (Ashkenazi Jewish ancestry)
  • Increased life time estrogen exposure
75
Q

For high risk patients to reduce breast cancer you would treat by… why?

A
  • use breast cancer receptor modulators like Tamoxifen and Raloxifene
  • reduces Estrogen Receptor (ER+) Breast cancer
76
Q

Stage 0-

A 
In situ (lobular or ductal)
-Treated with tamoxifene and raloxifene (lobular)

-Breast conserving surgery and radiotherapy (ductal)

77
Q

Stage 1 and 2

A

early invasive

-treated with breast conserving surgery +radiotherapy with systemic chemo

78
Q

Stage 3

A

locally advanced

-Induction of chemotherapy to reduce the tumor size followed by surgery and radiation therapy

79
Q

Stage 4

A
  • Metastatic
  • treated with just radiation therapy and systemic therapy

-23% chance of survival for 5 years with treatment

80
Q

Luminal A and B tumors

A
  • majority are ER+ HEr2- and have better prognosis. (70%)

- Luminal A has a better prognosis than B

81
Q

Her2 tumors

A
  • have a bad prognosis (ER-, Her2+)
82
Q

Gene Expression Profiling techniques for Breast Cancer

A

Oncotype DX (RT -PCR of 21 genes)

and

Mammaprint (DNA microarray of Frozen tissue of 70 genes)

83
Q

With the Oncotype DX Study results showed

A

basically the ODX results made no recommendation on chemotherapy recommendations

84
Q

80 percent of breast cancers are … 20 percent are…

A

sporadic,… familial

85
Q

HEr2

A

-is proto-oncogene that is a receptor tyrosine kinase.

It is converted to oncogene via gene amplification. (can be detected via FISH and CISH)

86
Q

Her2 treatment

A

Herceptin - Trastuzumab (extracellular action)
Lepatinib (intracellular action)

Trastuzumab-DM1 -anti-microtubule chemotherapy

87
Q

Maternal Serum Quad Test

A
  • 10-13 weeks gestation

- 4 different substances (ie.HcG, AFP ) used to detect abnormalities (80 percent detection for risk of Down syndrome

88
Q

To calculate the rate of the reaction (V) the equation is:

A

v= vmax*([S]/[S]+Km)

89
Q

To calculate the Km the equation is:

A

=k2+k3/k1

=[S] at which you have reached 1/2 vmax

90
Q

To calculate Vmax the equation is

A

k3(Et)

91
Q

To calculate the fraction of ES at any concentration f[ES]

A

v/vmax
which equals
=[S]/[S]+km

92
Q

To calculate kcat the equation is

A

vmax/Et
and
=k3

93
Q

To measure the ki the equation is

A

(E)(I)/(EI)

94
Q

In regard to an effective protease Inhibitor to work the best it must be able to fit into the protease active site by

A

matching substate transition state conformation and have low Ki

95
Q

In micro-satellites, repetitive bands in cancer tissue resulting from Chromosome breakage syndromes such as (HNPCC) indicate

A

-errors (mutations) or defect in DNA Repair mechanism causing the number of repeats

96
Q

what is the enzymatic equation for efficiency?

A

-kcat/km

  • kcat describes how much ES is used
  • km describes how much ES complex is available
97
Q

For a HIV protease to be resistant to an inhibitor, you have to have a

A

-higher Ki than the wild-type and near in kcat/km than the wildtype

98
Q

on the lineweaver-burk plot you have x intercept equal to

A

-1/km

99
Q

on the lineweaver-burk plot you have y intercept equal to

A

1/vmax

100
Q

on the lineweaver-burk plot you have slope equal to

A

Km/vmax

101
Q

why do we do enzyme assays at saturating substrate?

A

at this point change in substrate concentration is linear with change in product and

also

velocity (vmax) would be directly proportional to enzyme concentration. (Vmax=Et)

Biology (10 decks)

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