Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Cell Comm > Exam 4 > Flashcards

Exam 4 Flashcards

(77 cards)

Start Studying
1
Q

Normal blood glucose levels are determined by 2 factors

A

The release of glucose from the liver

And the uptake of glucose from adipose and skeletal muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Type I Diabetes

A

Inability to produce and release insulin due to an autoimmune destruction of the insulin producing B cells in the islet of langerhans in pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Type II Diabetes

A

Decreases the ability to produce and release insulin, associated with obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Glucose transporter protein also known as

A

Glut 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

In abscense of insulin

A

Glut 4 is sent to cytoplasmic vesicles and glucose cant enter the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

In presence of insulin

A

Vesicles with glut 4 are sent to the cell surface and fuse with the plasma membrane. Glut 4 is then inserted in the plasma membrane and glucose is transported into the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

To move Glut 4 to the plasma membrane what must happen

A

A signal from the insulin receptor will activate PI3 kinase and protein kinase B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is phosphotidyl inositols

A

Membrane lipids that locate on the inner leaflet of the phospholipid bilayer

Has unique kinase for phos hydroxyls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What position does PI3 Kinase phos Inositol

A

At the 3 position

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

The 3 phosphorylated inositols act as

A

2nd messengers, note all others have phos protein here it is a lipid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Structure of PI3 kinase

A

Has a catalytic subunit, an n terminal site to interact with reg subunits, a RAS binding domain which contain c2 domain which interact with lipid bilayer, and a helical domain which is what the rest of the domains lie on

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

The p85 aka N terminal sH3 domain allows for

A

Interaction with adaptor proteins. There are also 2 SH2 domains allowing for tyrosine kinase receptor. Site of interaction is sandwiched between the 2 SH2 domains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the role of p 85 in PI3 kinase

A

Allows catalytic domain to speak with appropriate cell components

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Protein kinase B (AKT) structure

A

Has plecstrikin homology domain allowing for interaction of PI3 phosphate lipids

Typical kinase domain. PI3 works by phos inositols giving PI3 phosphate lipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does Protein Kinase B work (PKB)

A

Interacts with PI3 phosphate lipids by it pleck homology domain and brings it to the plasma membrane where it can interact with PDK1. PDK1 is also brought to membrane by interaction of Pleck domain and phosphate lipids. PDK1 phos PKB in activation loop. Then PDK2 phos substrate binding domain and activate pkII. The activated PKB detaches from membrane and P target on ser/thr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does insulin stimulate PKB activity

A

Got deleted look in notes slide 50 on PI3 kinases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does vesicles dock

A

By a snares located in the target membrane and v snares located in the vesicle membrane they form coiled coils. Snares twist around each other and pulling membranes until they fuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Vamp is a v snare localized to

A

Glut 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

AS160 contains

A

Gtpase activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Mechanism of glut 4 vesicle fusion absence of insulin

A

In the absence of insulin the as160 it stimulates Gtpase of the RABs involved in the the ring of the glut 4, this maintains the RABs in a gdp state and inhibits the ability to tether glut 4 with the plasma membrane no glucose up take

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

In the presence of insulin

A

PI3 kinase pho phos inositols. PLC beta interacts with pi3 lipids and is P by PDK2 and PDK 2 which activates PKB and detaches it from the membrane and phos as160 resulting in coco change that inhibits gap activity GTP bound RABs and now glut 4 tethers to plasma membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Once insulin is activated

A

It phos munc 18 and it dissociates from syntaxin 4 and vamp 2. It docks and membrane fuses glut 4 is then inserted into the plasma membrane and imports glucose thus decreasing blood glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Roles of cellular adhesion molecules

A

Serves as receptors for extracellular signals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Two types of cell adhesion molecules

A

Homophillic and heterphillic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is linker dependant binding
Molecules are adjacent or linked to one another traveling via multivalent linker molecule
26
4 major groups of cellular adhesion molecules
Cadherin Selectins Ig like cams ] Integrins
27
Mediate calcium dependant cell cell interactions
Cadherins
28
Mediate transient calcium dependent cell cell adhesion interaction between blood and enodo cells
Selectins
29
Ig like cams
Mediate calcium INDEPENDANT cell cell adhesion
30
Inter grins
Mediate calcium dependent cell cell or cell matrix interactions and is always heterophillic
31
Cadherins absence and presence
Abscense of calcium proteins are floppy Presence of calcium stiff
32
Two classes of Cadherins
E Cadherins epitiheal cells N Cadherins neurons
33
Cadherin mode of action
Extracellular domain of Cadherin interact with extracellular domains of Cadherin dimers. Tails of the Cadherins are linked to actin filaments via anchor proteins called catenins. Which can cause comparisons and form polarized cells
34
So how do Cadherins compact
Actin gets depolarized and pulls in away from circle of actin tightens the interaction between all 8 cells compaction
35
3 types of selectins and function
P selectins platelets L selectins leukocytes E selectins endothelial cells Help regulate circulation of leukocytes between blood and infected tissues
36
Review integrins from paper second set of slides
Do it remember talin and shit
37
Part 3
Yay
38
What is the extracellular matrix
An organized network of proteins and polysaccharides in which tissue cells embed the self
39
Components of extracell matrix
Glycosamino gylcans (gags) Collagen Elastin Laminin
40
GAGs are and withstand compressive force how
Extremely hydrophilic due to negatvie charges of carbonyl and sulfates they attract cation which attract water to make gag gel allow tissue to withstand compressive forces
41
A type of fibrous protein is and resist stress
Collagen that can form a long stiff rodlike heli and their super helices assemble into collagen fibrils. The fibrils assemble into fibers They can resist tensile stress and serve as a highway for cell migration
42
Elastin (think elastic)
Composed of covalent elastic monomers and the monomers contain glycin sequence that allows them to stretch and recoil
43
The basal lamina contains
Laminin that function to provide a barrier to the move to of cells between tissue layers, highway for migration
44
A type of glycoprotein known as fibronectin
Has binding domains for interaction with gags integrins and has a collagen binding domain and a domain for associates with other fibronectin It functions to facilitate binding of cell to matrix and is a highway for cell migration
45
Role of ECM 4 components
Protection Cell migration Determine cell shape by actin and fibronectin Helps determine cell survival based on whether it is attached to the ECM (happy) not (dead)
46
Definition of apoptosis
Controlled cell suicide that cell will carry out in absence of certain survival factors
47
Characteristics of apoptotic cell
Disentigration of nuclear envelop Condensation of chromatin Lost of contact with ECM Blebbing of cell membrane —> apoptotic bodies Remnants eaten by macrophage Cell content not released into the environment
48
What mediates apoptosis
Caspases which are zymogens, enzyme in plasma. When inactive its called prolaspase
49
Caspases cleave proteins at
The consensus sequence
50
Auto cleavage
Cleavage by already activated caspase
51
Initiator caspases
Cleave and activate other caspases
52
Effector caspases
Cleave non caspase protein
53
How does first caspase become activated
Dimerization of the 2 pro initiator caspases which cleave and one another—apoptosis This is regulated by Bcl2 and BAD. Each of the initiator caspases are bound by an adaptor protein called Apaf. BCL2 will bind to apaf and prevent the dimerization of 2 pro caspases When a signal for apoptosis is sent BAD is activated and will bind BCl2 and pull it off apaf Apaf then mediates the dimerization of the 2 initiator caspases, they cleave and activate one another. The initiator caspases cleave and activate downstream caspases resulting in a caspase cascade and apoptosis
54
What do the caspases target
Laminin when cleaved breaks nuclear envelop Inhibition of cad when cleaved frees up caspase activated DNASE to chop cell DNA DNA repair enzymes
55
How binding of integrins to ECM prevents apoptosis
Extracellular fibroblast bind to fibronectin in ECM Intra cellular anchor proteins talin and vinculan bind cytoplasmic tails of integrin subunit. Bundle of actin bind to integrins to from focal adhesion complex Fak (focal adhesion kinase) associate with focal adhesion complex auto P and activate FAK PI3 kinases use SH2 domain to bind P FAK which generates Pip3 lipids resulting in recruitment and activation of protein kinase B. P of downstream targets and inhibits apoptosis
56
Anti apoptotic targets of PKB
Bad P and inactivate BAD. Bad cant interact with BCL2 no dimer of pro caspase P and inactivate initiator caspase P of txn factor FKHRL1 causing it to stay in cytoplasm. This txn factor activates proteins necessary to trigger apoptosis
57
How lose of integrins contact with ECM mediate apoptosis (cell death)
When integrin detach from fibronectin in ECM there is loss of interaction between integrin tail and actin Loss of contact result in conformational change in tail of integrin that allow interaction with initiator caspase Untethered integrins cluster the membrane results in cluster of procaspase which cleave one another and cause apoptosis
58
Receptors two types
Intracelluar entire receptor ftn as txn factor Is membrane bound then activation cleaves cytoplasmic tail and the cleaved tails serve as txn factor
59
Ligands such as lipophillic hormones include 3 types
Sex steroid Gluco corticoides Thyroid hormones
60
Primary response of receptor
Bind hormones to receptor leadin to activation of txn of few specific genes Carrier proteins will drop off hormones at destination-> hormones diffuse across the membrane of the target-> bind to receptor in cytoplasm-> dimerization-> change in receptor conformation-> reveal signal-> movement of ligand bound receptor to nucleus-> bind response element-> recruit coactivator-> activation of txn of gene
61
Structure of receptor
Has 5 regions Ab -> n terminal domain C dna biding domain Hinge region nuclear local signal E ligand binding domain F hormone dependant trans activation of txn
62
Secondary response of receptor
Proteins synthesized as a result of the P response are txn factor and induce another wave of txn
63
Thyroid hormone receptors what does its hormone system do
Regulate metabolism and neural development Hypothalamus release thyrotropin releasing hormone (TRH) primary TRH carried to pitiutiary activates thyrotrophs and relases thyroid stim hormone (TSH) secondary TSH carried to thyroid relases T3 and T4. Tertiary
64
Thyroid hormones regulated by
Negative feedback. Increase levels of T4 and T3 they will double back and inhibit their further release. Stop release from hypothalamus or anterior pituitary
65
If t3 and T4 of thyroid low then
Abnormalities Embryonic development then dwarf or decrease cognitive ability. Cretinism Adult Decrease metabolism and body temp. Myxedema
66
If T3 and T4 too high then
Graves’ disease actually a immune disease (causes high) resulting in low weight and high metabolism
67
Zinc finger family
2 sided finger with a zinc ion in the middle. One side is short alpha helix and the other is a 2 stranded beta sheet. Have fingers Thant grab and Bind DNA grooves
68
Ligand binding
Ligand binding domain consist of 12 alpha helices arranged in 3 layers. When unbound helix 12 extends from the ligand binding domain core Ligand will bind, and helix 12 fold back toward the ligand binding domain and aligns helix 3 and 4. The loop located between helix 2 and 3 flips under helix 6 completing fold around ligand leading to txn activation
69
What happens in txn activation
The hydrophobic cleft contain helix 3 and 5 and 12 recruit co activator histone acetylation leading to chromatin remodeling. Opens dna allowing This activates txn
70
Cleaved receptors overview of noth signaling
Notch receptors
71
Notch receptors are
Transmembrane receptors that play role in development
72
Notch receptors will bind insoluble ligand on the surface of nearby cells
The binding of ligand to notch result in cleavage of the receptor (notch) and release cytoplasmic tails The tails located to the nucleus and associate with DNA binding protein This form # of txn activators and activation txn of special genes
73
Notch 1 has 2 cleavage sites
S1 and S2 Transmembrane cleavage site at s3
74
Steps in Notch signaling
During trafficking to cell surface, notch 1 is cleaved in the heterodimer domain at S1 When ligand binds to the EGF repeats of NOtch 1 there is a conformation change that exposes s2 for cleavage by metalloprotease. (S2 would be protected in off state by LNR wrapping around its domain) Intermediate is cleaved at site 3 by secretase protease release active form of notch 1 Intracelluar notch 1 locates to nucleas and forms a txn complex with C3L and cofactors of the mastermind like family (mamL) MamL recruit additional cofactors and activate txn of genes harboring C3L binding site
75
How is a receptor degraded
ICN has short half life and when txn occurs P of pest degranulation domain causes ubiquitin at ion and Proteasome degradation.
76
Role of Notch 1 in T lymphocytes
t lymphocytes mature in thymus. During development the cells signal using NOtch 1 resulting in txn of a gene that encodes for pre t alpha chain and assembly of pre T cell at cell surface-> rapid proliferation and differentiation
77
Role of Notch 1 in T cell acute lymphocytic leukemia (T all)
In “all” the lymphocytes are unable to differentiate into mature cells and stay in lymphoblast stage. Most t alls have mutations. If signaling is not regulated of pre T cell then proliferation of undiffertiated cells

Cell Comm (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions