Introduction to Path

Question 1

HAT vs. HDAC proteins

Answer 1

HAT (histone acetyl transferase): opens up chromatin to allow gene translocation (euchromatin)
HDAC: removes acetyl group causing histone to close up chromatin (heterochromatin), which prevents gene translocation.

Question 2

Types and function of Non-coding mRNA

Answer 2

miRNA: used in post translational silencing

lncRNA: modulate gene expression, ie XIST gene, which turns off X chromosome making Barr body.

Question 3

Phosphatidylinositol

Answer 3

Found on the inner membrane
Used for protein scaffolding for intracellular proteins
PLC can break it down to make IP3 and DAG

Question 4

Phosphatidylserine

Answer 4

Found in the inner membrane
If it is on the outer membrane it becomes a cell marker for phagocytosis.
Cofactor for platelet activation

Question 5

Cancer type if … is found in high concentration

Lamin A, B, and C
Vimentin
Desmin
Neurofiliments
Glial fibrillary acidic protein

Answer 5

Lamin=nuclear lamina in calls

Vimentin= mesenchymal cells (fibroblasts/endothelium)

Desmin: skeletal muscle

Neurofiliments: Axons of neurons

Glial fibrillary acidic protein: glial cells around neurons.

Question 6

Progeria

Answer 6

When a person gets premature old age because of a lamin mutation

Question 7

Dynein vs. Kinesin

Answer 7

Dynein: retrograde transportation (to nucleus)

Kinesin: anterograde transport (away from nucleus)

Question 8

Cystic Fibrosis

Answer 8

CFTR defect: chloride channel defect

Protein can’t fold properly, can trigger ER stress response

Question 9

I-cell disease

Answer 9

Golgi is unable to put Mannose 6 phosphate on the vesicle, so the enzymes can’t be sent to the lysosome.
Patient will die due to lack of function of white blood cells.

Question 10

Warburg effect

Answer 10

Increased uptake of glucose and glutamine in cells but a decreased net ATP made per glucose molecule break down because carbon units being diverted to cell division prerequisites (HMP shunt pathway).

This happens in normal cells in G1/G2 phase and in cancer cells.

Question 11

Necrosis

Answer 11

Cell death by disruption of the mitochondria.

The mitochondria leaks into the cell causing a drop in the pH, which leads to cell death.

Question 12

Apoptosis

Answer 12

Programed cell death, which can be caused by

Cytochrome C release (inhibition of BLC-2)

Question 13

Receptor Type for insulin

Answer 13

RTK

Question 14

Growth factors likeEGF, PDGF, TGF… use which receptor type?

Answer 14

RTK

Question 15

HER2 mutation (ERBB mutation)

Answer 15

Leads to breast cancer

Question 16

HGF (scatter factor)

Answer 16

Mitogenic effects on hepatocytes, epithelial cells, biliary, pulmonary, renal, mammillary, and epidermal cells.
Plays a huge role in development and cell migration
Produced by mesenchymal cells, endothelial cells, and liver cells.

Question 17

PDGF: function & origin

Answer 17

Made from platelets, macrophages, endothelium, and smooth muscle

Function: proliferation for fibroblast, endothelial, and smooth muscle.

Question 18

VEGF

Answer 18

Protein involved in angiogenesis of blood vessels. It is also used in lymphocyte development, vascular dilation, and permeability.

Question 19

FGF

Answer 19

Associated with heperan sulfate in ECM

Used for wound healing, hematopoiesis, and development.

Question 20

TGF-Beta (fibronective agent)

Answer 20

Functions: activate bone morphogenic protein (BMP), activins, inhibins, and mullein inhibiting substance.

Origin: platelets, endothelium, and mononuclear inflammatory cells (B/T cells)

Too much will cause hypertrophic scars, systemic sclerosis, marphans syndrome, and a strong anti-inflammatory effect.

Question 21

GPCR MOA 3 types

Answer 21

Gq:causes activation of PLC, which makes IP3 and DAG,
Gs: formation of cAMP, which causes phosphorylation of proteins in the cell.
Gi: inhibits aldenylyl cyclase, which prevents the activation of cAMP.

Question 22

Basement membrane components

Answer 22

Collagen type 4, proteoglycan, and laminin.

Question 23

RTK MOA

Answer 23

Akt, MAP-kinase (Ras/Raf), and IP3 pathway.

Question 24

Collagen type 1: Origin & Defect

Answer 24

Origin: Bones

Defect: Osteogenesis Imperfecta and Ehlers-Danlos syndrome

Question 25

Collagen Type 2: Origin & Defect

Answer 25

Origin: Cartilage, intervertebral disks

Defect: Achondrogenesis type 2, spondyloepiphyseal dysplasia syndrome.

Question 26

Collagen type 3: Origin & Defect

Answer 26

Origin: Hollow organs and soft tissue

Defect: Vascular Ehlers-Danlos syndrome

Question 27

Collagen type 4: Origin & Defect

Answer 27

Origin: Basement membrane

Defect: Alport Syndrome

Question 28

Collagen type 5: Origin & Defect

Answer 28

Origin: Soft tissues, blood vessels

Defect: Classical Ehlers-Danlos syndrome

Question 29

Collagen type 7: Origin & Defect

Answer 29

Origin: Anchoring fibrils at dermal-epidermal junction

Defect: Dystrophic epidermolysis bullosa.

Question 30

Marfan syndrome

Answer 30

Defect in fibrillin

The patient will be very tall and lanky (Abraham Lincoln), they will have ectopic lens, and cardiovascular symptoms.

Question 31

Rb gene: function

Answer 31

Function is to prevent the cell from advancing into S phase.

Defective will lead to retinoblastoma.

Question 32

p53 function

Answer 32

Function: guardian of the genome, prevents cell from leaving G1 phase

Question 33

Niche cell

Answer 33

Special type of microenvironment in which somatic stem cells live in.

Question 34

Where are liver stem cells found?

Answer 34

Canal of Hering

Question 35

Where are the brains neural stem cells found?

Answer 35

Subventricular zone and dentate gyrus of the hippocampus.

Question 36

Labile cells

Answer 36

Cells that are continuously dividing (hematopoietic stem cells)

Question 37

Stable cells

Answer 37

Cells that can divide but a limited amount of division (generally in G0 phase, liver)

Question 38

Permanent cells

Answer 38

Cells that don’t divide (cardiac cells, stuck in G0).