Cell Bio IV

Question 1

Phospholipid Synthesis

Answer 1

• ends up being uneven with more on the cytosol side.

- Scramblase fixes this problem

Question 2

atlastin

Answer 2

a GTPase. Protein inboled in constructing and shaping Er

Question 3

What happens if there is too much atlastin

Answer 3

Increased ER membrane fusion and normal golgi is absent

Question 4

What happens if there is too little atlastin

Answer 4

ER becomes fragmented, possibly hereditary spastic paraplegia

Question 5

Symptoms of Hereditary spastic paraplegia

Answer 5

leg stiffness, gait disturbances, mental retardation, unique facial features

Question 6

Proeasomes

Answer 6

located in cytosol and nucleus, remove misfolded proteins. Can use ubiquition to help direct molecules to proteosomes by adding a tag. Require ATP

Question 7

Parkinson Diseas

Answer 7

Defective uniquitation of proteins

Question 8

Cystic Fibrosis

Answer 8

proteosomes destroy functional CFTR

Question 9

Proteasomes and cancer

Answer 9

Can be useful in treating cancer (multiple myeloma). Drugs inhibit proteasomes, trigger apoptosis in cancer cells

Question 10

Golgi apparatus

Answer 10

• Modifies and packages proteins into vesicles
• Sorts via chemical zip codes (linear sequence of amino acids, carbohydrate moieties)
• Membrane bound and close to the nucleus

Question 11

Kayser-Fleischer ring

Answer 11

Cu deposition in Descement’s membrane of cornea. Present in Wilson disease

Question 12

Wilson Disease

Answer 12

• defective transportor, can’t make ceruloplasmine, which leaded to a decrease in serum level ceruplasmine.
• Copper builds up in liver (may do so unevenly, so do more than one biopsy)
• Fatty accumulation in liver, low bilirubin value

Question 13

Mutation in Dysferin can cause what 3 types of muscular dystrophy

Answer 13

• miyoshi myopathy
• limb-girdle muscular dystrophy type 2b
• distal myopathy tibialism anterior muscle onset

Question 14

Golgi Appartus and insulin secretion

Answer 14

1. rER makes preproinsulin which is cleaved by microsomal enzymes
2. Nucleus makes mRNA for preproinsulin production
3. Small transfer vesicles transport proinsulin to golgi
4. Golgi packages proinsulin into coated secretory granules, converts proinsulin to insulin via prohormone converting enzymes
5. Secretory granules condense and store insulin

Question 15

Proinsulemia

Answer 15

• Mutated proinsulin is missorted, keeps getting produces

- Not enough proinsulin converting enzyme activity in unregulated pathway to deal with it

Question 16

Possible fates of endocytosed receptors and ligand

Answer 16

• Receptor is recycled, ligand is degraded
• Receptor and ligand are recycled
• Receptor and ligand are degraded
• Receptor and ligand are transported across the cell and are secreted (transcytosis)

Question 17

Achondroplasia

Answer 17

Due to recycling FGFR3 back to surface, amplifying the signal

Question 18

Lysosomes

Answer 18

very acidic, attract acid dyes

Question 19

Autophagic pathways

Answer 19

cell eats itself. Helps get rid of additional membrane that is no longer needed

Question 20

Heterophagosomes

Answer 20

gets rid of something from outside of the cell.

Question 21

Primary lysosome

Answer 21

all one color

Question 22

Secondary lysosome

Answer 22

Hetergenious