Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

MCM > Exam 1 > Flashcards

Exam 1 Flashcards

(134 cards)

Start Studying
1
Q

Vorinostat

A
  • A histone deacetylase (HDAC) inhibitor
  • In cancer, HDAC’s can be turned ON, and genome is turned OFF
  • This can turn ON the genome, in particular tumor suppressor genes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Werner Syndrome

A
  • Progeria syndrome (pre-mature aging)
  • WRN mutation
  • Helicase assoc. with telomere maintenance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Antimetabolites

A
  • Type of anti-neoplastic agent

- Incorporated into growing DNA instead of dNTP’s

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

Topoisomerase inhibitors

A
  • Type of anti-neoplastic agent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

RNA Polymerases

A 
mRNA - II
miRNA - II
tRNA - III
rRNA (5.8S, 18S, 28S) - I
rRNA (5S) - III
snRNA and scRNA - II and III
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Proteosomes

A
  • 20S core (protein breakdown)

- 19S caps (targets poly-ubiquitin tags)

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

Ubiquitin Ligase

A
  • find degredation signal on target protein

- Adds ubiquitin tag

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Actin

A
  • Most abundant cytoskeletal protein
  • G actin = globular
  • F actin = filament
  • Polym. occurs at + end, depolym. at - end
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cell shape/movement

A 
Actin forms cell processes
   - Microvilli
   - Filopodia
   - Pseudopodia
Locomotion
   - Lamellipodia (+ end leads)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Spectrin

A
  • Actin binding protein
  • Assoc. with membrane lipids/proteins
  • Anchors actin to membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Microtubules

A
  • ALPHA and BETA (form tube)
  • GAMMA (forms foundation)
  • Polym. at + end, requires GTP
  • Depolym. at - end
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Microtubule Organizing Centers (MTOC)

A
  • places in cells where microtubules start to form
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Microtubule Basal Bodies

A
  • part of MTOC
  • found at base of cilium/flagellum
  • allow for whip-like, unidirectional motion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Motorproteins

A
  • walk along microtubules
  • kinesins: walk to +, away from nuc, can push OR pull
  • dyneins: walk to-, towards nuc, can ONLY pull
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Intermediate filaments types

A

mechanical strength
assoc. with membranes and cytoskel.
types
- keratins (synth. by epithelium)
- neurofilaments (support long, thin axons)
- lamins (undelying all nuc membranes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Intermediate filament assembly

A
  • homodimers (two together)
  • protofilaments (two of those)
  • filaments (eight of those)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Desmosomes

A
  • cell-cell junctions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Hemidesmosomes

A
  • cell-ECM junctions (at basement membrane)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Basement membrane

A
  • Basal Lamina + Reticular Layer

- a fibrous EC layer

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

Glucosaminoglycans (GAG)

A
  • sugars with sulfate groups
  • (-) charged, trap + ions and water
  • part of proteoglycan (protein + GAG)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Propyl hydroxylase

A
  • resident ER protein
  • forms hydroxy-Proline from Proline
  • needed for collagen
  • REQUIRES Vitamin C (Scurvy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Collagen

A
  • 31 kinds
  • Sequence is Gly-Pro-hydroxyPro
  • makes triple helixes (tropocollagen)
  • important in wound healing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Elastin

A

can stretch and recoil
made of
- elastin (randomly coiled and hydrophobic, covalently cross-linked to each other)
- fibrillin (a surrounding network of microfibrils)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Lysyl oxidase

A
  • enzyme that does the cross-linking of elastin molecules to create elastin fibrils from tropoelastin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Fibronectin
``` principle adhesion protein in conn. tissue contains multiple adhesion domains - collagen - GAG (part of ground substance) - integrin (cell surface protein) ```
26
Laminin
- principle adhesion protein of basal lamina
27
Integrins
- cell surface receptors - bind to ECM (collagen, fibronectin, laminin) - anchor to cytoskel.
28
Focal adhesions
- attach motile cells to ECM | - anchor to actin skel.
29
Scurvy
defective collagen formation - impaired wound healing - capillary hemorrhage - vit C deficiency (ascorbic acid)
30
Kinetochore microtubules
- attach to sister chromatids | - depolymerize
31
Astral microtubules
- attach to membrane | - polymerize
32
Cell cycle: Restriction point
- late G1 - controls cell cycle and entry into DNA duplication - Is environment favorable?
33
Cell cycle: G2/M checkpoint
- during G2 - is all DNA copied? - Is environment favorable?
34
Cell cycle: Metaphase-to-anaphase checkpoint
- During M | - Are all chromosomes attached to spindle?
35
Cell cycle: DNA damage checkpoints
Found in - G1 - S - G2
36
Cyclin dependent kinases
Phosphorylate proteins that regulate cell cycle G1/S cyclin - trigger progression through restriction point - peaks in G1 S cyclin - trigger chr duplication - Peaks through S and G2 M cyclin - trigger process through G2/M checkpoint - Peaks in M
37
Regulation of Cyclin-Cdk complex - Cdk-activating kinase - Wee1 - Cdc25 - Cdk Inhibitor proteins (CKI)
Cdk-activating kinase (activates complex by P active site) Wee1 (inhibits complex by P inhibition site) Cdc25 (actiates complex by de-P inhibition site) Cdk Inhibitor proteins (CKI) - creates Cyclin-Cdk-CKI complex - inhibits Cyclin-Cdk activity - ex: p27, p21, p16
38
Securin
- hold sister chromatids together
39
APC/C
- anaphase promoting complex/cyclosome - actived by Cdc20 - ubiquitin ligases target securin (hold sister chr together) for degradatin -------> anaphase
40
Origin replication complexes
- complexes found at origins of replication - remain assoc. with origins throughout cell cycle - include DNA helicases - these are Phosphorylated to initiate replication
41
Cohesins
- ring-like structures around sister chr to keep them together - cleaved by separase
42
M phase control
M-Cdk Phosph. targets - Condensin (promotes chr condensation) - Mitotic spindle - Nuclear pore complexes - Nuclear lamina - APC/C
43
[Glucose] in cell
- 5mM | - 90 mg/dL
44
Phosphofructokinase
- 3rd step of Glyc. - F6P ------> F-1,6-BP - Activated: AMP, F-2,6-BP - Inhibited: ATP, citrate
45
Hexokinase (I and IV)
``` Commitment step of Glyc. Glu -----> G6P Inhibited by G6P (product) Hexokinase I - high affinity, low Km - NOT super specific for Glu - Inhibited by its product Hexokinase IV - "Glucokinase" - In liver and pancrease - NOT inhibited by G6P - Larger Km, though - highly specific for Glu - Acts as a sensor for B-cells in pancrease (high Glu --> more HK IV activity --> insulin secreted) ```
46
Pyruvate Kinase
- 10th step of Glyc. - PEP -----> Pyruvate - Activated: AMP, F-1,6-BP - Inhibited: ATP, Acetyl-CoA
47
Arsenic
Found in - Rat poison - Herbicides - Industrial cleaners Inhibits Pyruvate Dehydrogenase (Pyruvate ---> A-CoA) "Garlic smell" = PDH deficiency = lactic acidosis
48
Carboxylases
``` Require ABC - ATP - Biotin - CO2 Pyruvate carboxylase (gluconeogen.) Acetyl-CoA carboxylase (FA synth.) Propionyl-CoA carboxylase (Prop. acid pathway) ```
49
TLCFN
``` TLCFN - TPP (thiamin, Vit B1) - alpha-Lipoiic Acid - CoA - FAD (riboflavin, Vit B2) - NAD+ (nicain, Vit B3) 3 enzymes require - Pyruvate DH (pyruv ---> A-CoA) - a-ketoglutarate DH (a-KG ---> succinyl CoA) - branched chain ketoacid DH (Val/Iso/Leu ---> Propionyl CoA) "maple syrup urine disease" ```
50
Hutchinson-Gilford Progeria Syndrome
``` normal dev. 3-6 months LMNA mutation - Lamin A, of nuc. lamina fragile nuclei, genomic instability mean death 13.5 years ```
51
Beriberi
``` Thiamine deficiency (Vit B1) Need TPP for TLCFN enzymes - Pyruvate DH - a-Ketoglutarate DH Loss of neural function ```
52
Fluoroacetate
- Inhibits aconitase of TCA cycle - metabolizes to fluorocitrate - in some acacia trees in Australia/Africa
53
Tyrosine-Kinase Associated Receptors
``` act through CYTOplasmic tyr. kinases soluble tyr. kinases in cytosol associate with activvated receptor ligands - cytokines - interleukins - integrins ```
54
Receptor Tyrosine Kinase
``` aka "Tyrosine-linked receptors" contain intracellular tyrosine kinase domain two monomers cross-Phosph. each other ligands - growth factors ```
55
Philadelphia chr
- chromosomal translocation - Bcr-Abl fusion protein - Abl is always ON (it's a Tyr Kinase) - chronic myeloid leukemia - treated by Imatinib (Gleevac)
56
PDGFR
``` platelet derived growth factor receptor stimulated mitogenic activity (MAPK/PI3K) oncogenic mutation - chronic myeloid leukemia - GI stromal tumors ```
57
GSD Type 1
``` von Gierke's Glu-6-Phosphatase symptoms - severe hypoglycemia - hepatomegaly - hyperlipidemia ```
58
GSD Type 2
``` Pompe's acid a-glucosidase (a1-4 linkages) symptoms - cardiomegaly - death by 2 y/o ```
59
GSD Type 3
``` Cori glycogen debranching enzyme/glycogen phosphorylase symptoms - mild hypoglycemia - hepatomegaly ```
60
GSD Type 4
``` Andersen Glycogen branching enzyme Symptoms - cirrhosis - failure to thrive - hypotonia - death by 2 y/o ```
61
GSD Type 5
``` McArdle's Muscle glycogen phosphorylase Symptoms - muscle weakness - cramps on exercise - rhabdomyolysis ```
62
GSD Type 6
Hers Liver glycogen phosphorylase Symptoms - hepatomegaly
63
Ion Flow (Na, Ca, H, K, Cl, HCO3)
``` In - Na - Ca - H Out - K - Cl - HCO3 ```
64
Wernicke-Korsakoff Disease
brain syndrome cause by lack of Vit B1 (thiamine) transketolase has low affinity for TPP due to point mutation (part of HMP Shunt) symptoms - ataxia - psychosis - confusion Also, alcohol inhibits thiamine absorption
65
Citrate synthase
``` A-CoA + Oxaloacetate ---> Citrate (Krebs) Inhibited - citrate - succinyl-Coa - NADH - ATP (this can be reversed by AMP) ```
66
Pyruvate DH
``` Pyruvate ---> Acetyl-CoA TLCFN Activated: - NAD+ - CoA - Ca (in muscle only) Inhibited - A-CoA - ATP - NADH ```
67
Complex 1 (ETC)
- NADH-ubiquinone oxidoredutase
68
ETC/OP Inhibitors (I - 2, IV - 3, OP - 2) | - "Br-cac, DO"
``` Complex I - Barbiturates - Rotenone (fish poison) Complex IV - Cyanide (Fe3+) - CO (Fe2+) - Azide ATPase - Oligomycin (antibiotic, plugs opening of F0) - DCCD ```
69
Chylomicrons
- packages of fat from diet | - Ride on Apoprotein B48
70
VLDL
- very low density lipopotein - it is made of excess Glucose from diet - Glu --> Pyruvate --> A-CoA --> fatty A --> fat (then exit liver) - drop off FA at adipose, return glycerol-P to liver
71
lipoprotein lipase
- cuts the FA's off of the fat in VLDL | - drops off FA at adipose tissue for storage, glycerol will return to liver
72
GLUT4
- Glu transporter - found in muscle and adipose - stays in vesicles, waiting for insulin to arrive at cell, then it's on surface
73
Main source of fuel, 4 hours after eating
Liver glycogen
74
Main source of fuel, `8 hours after eating
Fatty acids (adipose tissue
75
Main source of fuel, 5 days after eating
Ketone bodies | - Adipose tissue fat --> (b-ox) --> fatty a --> fatty a albumins --> Liver --> A-CoA --> ketone bodies
76
4 main starvation adaptations
1. fat hydrolysis in adipose 2. gluconeogenesis in liver and kidney 3. ketogenesis in liver 4. protein degridation in muscle
77
CTD Tail
C-terminal end of RNA Pol II | Must be phosph. to initiate transcription
78
DNA Methylation
Done at CpG islands (C's that proceed G's) Transcriptional REPRESSION Heritable (epigenetic)
79
siRNA
- small interfering RNA - can induce transcriptions silencing - usually exogenous (artifically introduced)
80
miRNA
- micro RNA - an regulate mRNA degredation by base pairing with existing mRNA, targets it for destruction - usually endogenous
81
GLUT2
Found in Liver and Pancreatice B-cells Uptake and release of Glu (liver) Glu-sensing (B cells) - GLUT2 --> ATP:ADP ratio --> membrane depolarization --> open Ca channel --> Ca enters --> Insulin vesicles secreted
82
3 different hemolytic anemias
1st most common Sickle cell - Hb has mutation --> distorts RBC --> RCB life expectancy drops --> RBC lysis 2nd most common Pyruvate kinase deficiency - Back up of Glyc. --> no ATP --> RBC has no other source of ATP --> can't power Na-K pumps --> cell hypotonic --> swells --> lysis G6PD deficiency - No entry into HMP Shunt --> can't make NADPH (reduced glutathione) --> oxidative damage to RBC --> lysis
83
MetHb
- Methemoglobin - Heme group has Fe3+ not Fe2+ - Cannot carry O2 - Reverted to Hb by MetHb reductase, which requires NADPH - "methemoglobinuminia"
84
Heinz bodies
Small budding dots on RBC's | Found in G6PD hemolytic anemia, but not PK
85
2,3-BPG
- Part of Glycolysis - Binds to Heme groups in Hb and lowers O2 affinity - Necessary for dumping O2 in tissue - It binds the B subunit of Hb and "kicks off" the O2 there - HbF (fetal) has alpha and gamma subunits, so unaffected by 2,3-BPG
86
Pyruvate Dehydrogenase
- Pyruvate to A-CoA - Inhibited by Arsenic (rat poison, herbicides, moonshine) - TLCFN Thiamine deficiency - common in alcoholics (alcohol inhibits absorption of thiamine) - and IV solution of glucose can kill alcoholics because lactic acidosis
87
Cell response to hypertonicity (in surroundings)
Activate Na-H exchanger (Na in, H out) ---> This activates Cl-HCO3 exchanger ---> Cl enters Net uptake of Na and Cl ---> water follows
88
Cell response to hypotonic (in surroundings)
Activate solute efflux (either Cl and/or K channels) ---> Water exits
89
Idiogenic osmolytes
Some cells can increase tonicity by producing these Response to long-term hyperosmolality OR because Na and Cl can interrupt cell processes
90
Na-H exchanger
"acid extruder" - Uses Na gradient to move H out - activated by intracellular metabolic acidosis - inhibited by very high pH - induces Cl-HCO3 exchanger by creating high pH
91
Cl-HCO3 exchanger
"acid loader" - uses Cl gradient to move HCO3 out - activated by intracellular metabolic alkalosis - inhibited by very low pH - induces Na-H exchanger by creating low pH
92
Intracellular respiratory acidosis
high E CO2 pushes CO2 into cell low pH in cell CO2 + H20 ---> H + HCO3 (carbonic anhydrase) Activate Na-H exchanger
93
Protein sorting signals
encoded in aa sequence usually at N-terminus or can be "signal patches", not near each other in aa sequence, but in 3d are near each other no signal = destined for cytosol
94
Importins
Recognize nuclear localization signals on proteins Brings them to/through nuclear pore complex Have two binding sites - nuclear localization signal - nuclear pore complex
95
Exportin
Recognizes nuclear export signal RanGTPase binds the protein-exportin complex and exits the nuclear pore with them - RanGTPase used to dissociate the complex in the cytosol
96
Vesicle coats from different sources
Clathrin-coated (from plasma membrane) COP I-coated (from Golgi) COP II-coated (from ER)
97
ER retrieval signal
KDEL Usually at C-terminus Proteins can only leave ER after this sequence has been cleaved
98
SNARE
v-SNARE (vesicle) t-SNARE (target) Need SNARE-SNARE interaction for vesicle fusion
99
Co-translational import
rER "catches" the protein as it's coming out of the ribosome SRP recognizes the early budding protein, brings it to SRP receptor on ER Two types of proteins are usually co-translated - transmembrane proteins - water soluble protein (for secretion)
100
Lysosome maturation
Endocytotic vesicle ---> Early endosome ---> Late endosome (mildly acidi pH 6, zymogens) ---> Endolysosome (fusion with pre-existing lysosome, activates zymogens, pH 4.5-5) ---> lysosome
101
Mannose-6-P
Signals lysosomal proteins for lysosomes | M6P receptors are on the inside of Trans-Golgi
102
UDP-glucose phosphorylase
G1P ---> UDP-Glu (to be added to glycogen) | Required UTP
103
Glycogen synthase
UDP-Glu ---> Glycogen (a1-4 linkages) Activated by Insulin Works alongside Glycogen branching enzyme (a1-6 linkages, every 8-14 residues)
104
Gluconeogenesis
Mainly in liver/kidneys (only places with G6Pase) E to power gluconeogenesis comes from triacylglycerides (TG) Hormone Sensitive Lipase (HSL) breaks fat ---> FA + Glycerol
105
Cori cycle
LIVER Lactate ---> Pyruvate ---> Glu (gluconeogenesis) BLOOD Transport MUSCLE Glu ---> Pyruvate ---> Lactate * this cycle produces lactic acidosis
106
Glucose-Alanine Cycle
LIVER Alanine ---> Pyruvate ---> Glu (alanine transaminase) Urea excreted BLOOD Transport MUSCLE Glu ---> Pyruvate ---> Alanine (alanine transaminase)
107
Transketolase
Part of HMP Shunt Requires TPP (but not the rest of TLCFN) Wernicke-Korsakoff Disease (mut in TK gene, enzyme won't bind TPP) - treat with increased thiamine in diet (Vit. B1)
108
G6PD deficiency
Most common enzymatic deficiency in world X-linked recessive 10-14% of African-American males have it 1. Immunodeficiency - In neutrophil, no NADPH made 2. Heinz bodies - Hb denaturation in RBC's because oxidative damage because no reduced gultathione because no NADPH 3. Hemolytic anemia
109
Trophic factors
Cells require these signals to "keep living"
110
Cell signaling dessensitization
Receptor sequestration Receptor down-regulated Receptor inactivated Inhibitor protein production
111
Mitogen
Signaling molecules that stimulate cell division | Activate G1/S-Cdk activity
112
Intracellular receptors
1. Steroids - hydrophobic enough to diffuse in to cell - intracellular receptors dimerize and then go to nuc as TF's 2. Nitric Oxide - gas, small enough to diffuse - acts locally, short half life - Activates guanylyl cyclase (GTP ---> cGMP)
113
Eicosanoid
Lipids that bind cell surface recptors Short half life, act locally Induce clotting and inflammation
114
Ion-channel-coupled | "Ionotropic"
Rapid signaling in electrically-excitable cells Action: opens/closes ion channels to change excitability state of cell Ligands: Neurotransmitters
115
G Protein coupled receptors | GPCR
7TM (7 pass transmembrane proteins) Ligands: eicosanoids, neurotransmitters, peptide hormones Special senses: smell, sight, taste Coupled to three protein inside alpha (binds GTP) beta-gamma (they stay together) alpha subunit will be activated and will activate/inhibit adenylyl cyclase Gs (activates) vs. Gi (inhibits)
116
Receptor serine/threonine kinases
Ligands: TGF-beta Action: form heterodimers --> one chain activates other --> activates Smad pathway
117
Notch | - Do Not Work For HP
Receptor for direct cell-cell signaling Ligand: Delta Action: Delta induces proteolytic cleavage of cystolic tail of Notch ---> to nuc as TF
118
Frizzled | - Do Not Work For HP
Receptor Ligand: Wnt It stops the bully from phosphorylating and ubiquinating beta-catenin
119
Patched | - Do Not Work For HP
Receptor Ligand: Hedgehog Actions: Activated smoothened ---> inhibits phosphorylation of Ci ---> Ci becomes TF
120
Death receptors
Ligands: cytokines, growth factors, pathogen assoc. molecular patters (MAMP) Action: binding of one ligand induces clustering of cytosolic Death Domains Ex: Caspase
121
Inegrins
At cell-matrix junctions (focal adhesions, hemidesmosomes) | Induce proliferation, gene expression, survival
122
cAMP
A secondary messenger | Activates protein kinase A
123
PIP2
Cleaved by phopsholipase C into IP3 + DAG (two secondary messengers) IP3 - activated ligand-gated Ca channels DAG - activates protein kinase C
124
PI3 Kinase
Phosphorylates PIP2 to PIP3 This activate Akt, a kinase that influences cell survival and protein synth. A secondary messenger
125
JAK/STAT
``` JAK - cytokine receptor - non-receptor protein Tyr kinase - phosphorylates nearby STAT's ---> STAT's dimerize ---> TF's STAT - The secondary messenger ```
126
NF-kB
regulates proliferation and survival activates through death receptors Ligands: Cytokines, growth factors, pathogen assoc. molecular patters (MAMP) (this is same as death receptors) Action: Receptor activates 1kB kinase ---> phosphorylates and ubiquinates 1kB (which had been covering a NF-kB dimer) ---> free NF-kB dimer ---> TF It's a secondary messenger
127
Rho (secondary messenger)
Regulates cytoskeletal changes Activated through integrins, growth factor receptors Promotes actin growth, and phosphorlationg of myosin
128
Sickle Cell Disease | HbS
Affects shape/life span of RBC's Mutation in B chain, non-polar Val for Glu Creates hydrophobic knobs that aggregate and pcpt
129
Sickle Cell Symptoms
Anemia Growth failure - long term effect of anemia Infection - reduced splenic function Vaso-occlusive events - local vessel obstruction, further promotion of hypoxia/acidosis - causes extreme pain Organ failure - long term effect of hemolysis and clogging
130
Sickle Cell Treatment
Hydroxyurea - stimulates HbF production - mechanism noe 100% known but... - Activates NOS - ribonucleotide reductase
131
Ionotropic | receptor class
- ligand-gates ion channels | - typically fast neurotransmitters
132
Metabolic | receptor class
- G protein coupled | - coupled with effector protein, ion channel, or TF
133
Enzyme-linked | receptor class
- act on TF's | - cell growth, differentiation, division, apop., inflammtion
134
``` Nuclear receptors (receptor class) ```
- act directly as TF's | - located in cytosol/nucleus, ligand must diffuse in

MCM (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions