Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
37 Cards in this Set
- Front
- Back
phagocytosis
|
-cell eating; ingestion of bacteria, large particles or other cells
-occurs mainly in specialized cell types such as neutrophils and macrophages |
|
pinocytosis
|
-cell drinking; ingestion of solutes such as proteins, hormones and macromolecular complexes in liquid medium
-occurs in all cell types |
|
clathrin dependent pinocytosis
|
-receptor mediated endocytosis
-type of pinocytosis |
|
caveolae
|
-ingestion of small vesicles formed by aggregation of caveolin in lipid rafts
-type of pinocytosis |
|
macropinocytosis
|
-uptake of liquid in large vesicles formed by extensions of plasma membrane
|
|
4 main steps of phagocytosis
|
1. binding of material at extracellular surface of plasma membrane
2. extension of plasm membrane (pseudopodia) by microfilament-dependent movement 3. formation of large intracellular vesicles (phagosomes) by fusion of pseudopodia 4. fusion of phagosomes with lysosomes for enzymatic digestion (phagolysosomes) |
|
phagocytosis
|
-cell eating; ingestion of bacteria, large particles or other cells
-occurs mainly in specialized cell types such as neutrophils and macrophages |
|
pinocytosis
|
-cell drinking; ingestion of solutes such as proteins, hormones and macromolecular complexes in liquid medium
-occurs in all cell types |
|
clathrin dependent pinocytosis
|
-receptor mediated endocytosis
-type of pinocytosis |
|
caveolae
|
-ingestion of small vesicles formed by aggregation of caveolin in lipid rafts
-type of pinocytosis |
|
macropinocytosis
|
-uptake of liquid in large vesicles formed by extensions of plasma membrane
|
|
4 main steps of phagocytosis
|
1. binding of material at extracellular surface of plasma membrane
2. extension of plasm membrane (pseudopodia) by microfilament-dependent movement 3. formation of large intracellular vesicles (phagosomes) by fusion of pseudopodia 4. fusion of phagosomes with lysosomes for enzymatic digestion (phagolysosomes) |
|
Dynamin
|
GTPase in plasma membrane required for budding of clathrin coated vesicle from clathrin coated pits
|
|
structure/function of clathrin
|
-distorts plasma membrane by budding to produce vesicle
-captures membrane receptors and bound molecules Y heavy chain (arm) and light chain (internal) and binding site for assembly particles (hands) |
|
adapter proteins
|
-on inner coat of clathrin
-consists of adaptin subunits -provides specificity by coupling of receptor to clathrin coated pit |
|
what is recylced?
|
clathrin coat reforms transport vesicle that takes adapter proteins and receptors (after fusion with early endosome) back to plasma membrane
|
|
what occurs after internalization? -up to sorting
|
clathrin coat dissociates and fusion between vesicle and early endosome
-ligand and receptor dissociate -ligand (cargo protein) |
|
pH of lumen of early endosome how and what significance?
|
6.0
H+ pump lowers to this pH causes dissociation of ligand and receptor |
|
endocytic vesicles
|
-buds from early endosome
-carries ligand to late endosomes |
|
pH of late endosomes and significance
|
approx 5.5 then lowered to 5.0
-activates lysosomal hydrolases |
|
what occurs after sorting?
|
-endocytic vesicles fuse with late endosome
-lysosomal hydrolases from trans Golgi network (tagged with mannose-6-p, so sorting occurs for those without tag) in vesicles are fused with late endosome -late endosome lowers pH to 5.0, activating enzymes -recycling of endosome membrane proteins back to trans Golgi |
|
how are vesicles transported?
-note from Bradshaw lecture |
transported along microtubules using either dyne in motor proteins (towards minus end of MT) or kinesins (towards plus end of MT)
|
|
types of ligands (8)
|
hormones
growth factors lipoproteins antibodies vitamins iron binding proteins toxins viruses |
|
significance of multivesicular body
|
-ligand and receptor are degraded in lysosomes
-eg EGF (epidermal growth factor) receptor is tagged with ubiquitin -integral membrane protein (receptor in this eg) is sorted in to small vesicles in late endosome -accumulation of small vesicles gives rise to multivesicular body which fuses with lysosome and degrades membrane and associated proteins of the vesicles |
|
function of MVBs
|
-sorting and degradation of integral membrane proteins
-hormone desensitization by down-regulatoin of receptor |
|
caveloae structure/location
|
-invaginations of plasma membrane, 50-80 nm
-integral membrane proteins, NOT RECEPTOR MEDIATED -abundant in vascular endothelial cells, smooth muscle cells, fibroblasts and adipocytes |
|
caveolins molecular components
|
-integral membrane proteins
-type of lipid raft -cholesterol and sphingolipids microdomains, stabilized by caveolin proteins |
|
caveolins functions
|
-endocytosis- bud as vesicles from plasm memrane and fuse with either caveosomes or early endosomes
-transytosis- bud as vesicles from cell surface, traverse the cell and fuse with plasma membrane at another location on cell surface |
|
what protects lysosome from self digestion?
|
glycosylation of membrane proteins protects luminal surface of lysosome
|
|
what do lysosomal enzymes contain and how are they sorted?
|
contain N-linked oligosaccharides that are phosporlated in cis Golgi Network to generate Mannose-6-P tag
-Mannose-6-P binds to its receptor which binds to adaptor protein 1 on clathrin coat |
|
autophagy
|
self digestion of organelles and proteins by the cell
|
|
autophages
|
membrane bound vacuoles derived from ER, enclose organelles or cytoplasm
|
|
phagolysosomes
|
autophages fuse with lysosomes to form these which digest contents
|
|
what causes lysosomal storage diseases?
|
autosomal recessive disorder causes deficiency in lysosomal enzyme
-results in accumulation of undegraded substrates |
|
I-Cell Disease
-what are cellular defects? |
-defective processing of Mannose-6-P tag
-lysosomal enzymes not sorted by golgi in to clathrin coated vesicles bound for lysosomes -deficiency of multiple enzymes causes substrates to accumulate in cells and form inclusion bodies |
|
Tay--Sachs Disease
-what is the defective enzyme and what are the cellular defects? |
alpha hexosaminidase A
-accumulation of gM2 gangliosides in brain -causes increase in glial cells and abnormal growth of dendritic processes of neurons |
|
Gaucher's Disease
-what is the defective enzyme and what are the cellular defects? |
beta glucocerebrosidase
-accumulation of glucocerebroside in macrophages -leads to enlarged spleen and liver |