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37 Cards in this Set

  • Front
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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