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BZ 310- Final

Anterograde secretory pathway secretion or to the vacuole
Retrograde secretory pathway endocytosis
Smooth ER functions (3) detoxification (cytochrome P450), steroid hormone synthesis, Ca2+ storage
Rough ER functions (4) secretory protein synthesis/uptake, N-linked glycosylation, secretory protein folding, phospholipid synthesis
What does cytochrome P450 do? oxidizes harmful hydrophobic molecules
Cystic fibrosis malfunctioning ER functions
Nascent polypeptide Asn-X-Ser/Thr; core oligosaccharide attached to this, then 3 glucose later removed
O-liked glycosylation rare; usually n-linked
Enzymes that remove glucose from core oligosaccharide glucosidase (I and II)
ER quality control final glucose only removed when protein is folded correctly
Functions of glycosylation (6) enzyme folding, quality control, sorting, enzyme functionality, recognition at cell surface, protection at cell surface
Functions of Golgi (4) protein sorting, modification of N-linked sugar groups, O-linked glycosylation, formation of some cell wall components
How were the secretory mutants found in yeast? mutants sunk after centrifugation
Class I mutants defect in ER translocation
Class II mutants defect in vesicle budding from ER
Class III defect in fusion with Golgi
Class IV defect in budding from Golgi
Class V defect in fusion with plasma membrane
Two major processes in secretory pathway coat protein mediated budding & SNARE receptor mediated vesicle docking and fusion
Clathrin involved in receptor mediated endocytosis and transport to endosomes/lysosomes
COP II and COP I golgi==>ER
Rab a small GTPase needed to prime a vesicle
Transport to lysosome/plasma membrane depends on what? mannose 6-P
Polarized cells (4) epithelia, neurons, fibroblasts, T-cells
Two types of exocytosis constitutive and regulated
V-snares/T-snares mediate secretion by promoting vesicle docking and fusion
Female meiosis only keep 1 cell in meiosis 1, only keep 1 at meiosis II (right before fertilization)
G1 1 chromosome = 1 chromatid = 1 DNA
G2 1 chromosome= 2 chromatids= 2 DNAs
Interphase GI, S, G2
SERIOUSLY 14.11 all of the chromosome shit
Astral spindle MTs connect to periphery
Polar spindle MTs space spindle poles relative to each other
Kinetochore spindle MTs catch chromosome, connect to kinetochore
Metaphase chromosomes in center of cell
Anaphase chromatids separate
Telophase chromosomes de-condense, nucleus reforms
Most important control point in cell division START (between G1 and S)
What is checked at START? (3) cell size, DNA intactness, nutrient availability
G0 cells enter this when don’t need to divide; must enter G1 to divide again
CdK cyclin dependent kinase; each checkpoint has its own
Cyclin proteins that vary in concentration over the cell cycle
Example of cyclin and cdk pair MPF (mitosis promoting factor); conserved
2 main regulatory mechanisms of cell cycle phosphorylation (reversible), degradation of cyclins (irreversible)
p53 checks for DNA damage at start and G2-M transitions; transcription factor for cyclin inhibiting protein (=cell cycle arrest)
which 2 cell wall components are secreted and more soluble? pectin and hemicellulose
which 2 cell wall components are synthesized in place? cellulose and lignin *make up most biomass on earth
___ connect the cytoplasm of plant cells plasmodesmata
proteins in connective tissue are secreted by fibroblasts
proteoglycans function cushioning
collagen vitamin c dependent, stretching resistance
4 types of cell-cell connections adherens, gap, tight, desmosome
gap junctions 2x6 connexins= connexon (allow signaling like cAMP thru)
receptor connection to actin contraction, crawling
receptor connection to IFs stretching resistance
4 main cell surface receptor types cadherin, CAM, integrin, selectin
adherins junctions connect cells to cells, Ca2+ dependent
two cell connections not associated with cytoskeleton CAMs and selectins
CAMs Ig like, tissue specific (cell adhesion molecule)
Selectins recruitment of WBCs to infection site (example)
3 cell connections associated w/ cytoskeleton integrins, hemidesmosomes, focal contacts
integrins connected to actin, important in cancer biology/infection
hemidesmosomes connected to IFs, keratin
4 signal sending ways autocrine, paracrine, endocrine, direct contact w/ cell receptors
3 main cell receptor types in membrane ligand gated, GPCR, tyrosine kinase
3 major mechanisms of signal transduction phosphorylation/de, second messengers, GTP switches
3 types of second messengers cAMP, phosphatidyl inositol derived, Ca2+
cAMP signaling hunger/stress signals
PI 2nd messengers IP3 (Ca2+ from ER), DAG (activates PKC), PIP3 (activates PKB)
Ca2+ 2nd messenger activates calmodulin, troponin, etc.
All second messengers readily available source, removed quickly
Well known for short term responses GPCR
Well known for long term responses tyrosine kinase
PLC -> IP3 + DAG
Adenylyl cyclase -> cAMP
Gluconeogenesis cAMP example CREBP binds to CRE (cyclic amp response element)
Two different types of g proteins Gs (stimulate), Gi (inhibit)
Cholera toxin modifies Gs to cannot hydrolyze GTP, efflux of ions= diarrhea
Multiple second messengers example inositol metabolites can raise intracellular Ca2+ and activate PKC (smooth muscle contraction)
4 major off-switching mechanisms GTP hydrolysis, cAMP broken down by phosphodiesterase, Ca2+ pumped, phosphatases
Ras small GTP binding protein that functions as an on and off switch (MAPKKK)
EGF signaling RTK activity, c-fos/c-jun= TFs and proto-oncogenes
How cells know which cell to be transient activation of enhancer, protein expressed, positive feedback loop
Principle of apoptosis conserved; regulated activation of proteases called capases (zymogen)
Cancers from mesodermal origin leukemia, lymphoma, CNS, retinoblastoma, sarcomas
Characteristics of cancer cells (8) grow in clumps, altered growth factor response, invasion of other tissues, altered karyotypes, immortal, altered cytoskeleton, altered receptors, less adhesive/more motile
8 types of proteins that control cell growth growth factors, growth factor receptors, signaling cascade, cyclin dependent kinases/cyclins, protein kinases, chromatin proteins, transcription factors, proteins in apoptosis
tumor suppressors need to both be mutated (recessive); p53
oncogenes dominant, Ras
retrovirus and cancer can pick up a proto-oncogene and make it an oncogene
DNA virus and cancer interferes with normal replication controls
3 immune layers of defense mechanical/chemical, innate, acquired
innate responses (4) inflammation, phagocytosis, NK cells, complement
humoral immunity B cells -> antibodies, maturation in bone marrow, bursa in birds
cellular immunity cytotoxic T-cells, helper T-cells; maturation in thymus
IgG main blood antibody; complement activation
IgM B-cell antigen receptor or in blood; activates complement (before IgG)
IgA in secretions, dimer
IgD B-cell activation
IgE parasites, allergies
3 mechanisms of antibody diversity combine light + heavy chain, imprecise joining, hypermutation
MHC I all cells (pairs w/ CD8)
MHC II professional antigen presenting cells (pairs w/ CD4)
MHC I peptide binding domain same structure as HSP 70 (form fits function)
Tc kill what? all cells that present a foreign protein
Coordination of immune response by Th cells get out of G0 upon activation, stimulate B cells that display antigen on MHC II, then they get out of G0 (positive feedback)
Negative selection cells with strong recognition of self MHC (or cells with very weak recognition of MHC) -> cells killed (auto-immune)
Created by: melaniebeale