Docsity
Log inSign up
Docsity
Prepare for your exams
Prepare for your exams

Study with the several resources on Docsity

Earn points to download
Earn points to download

Earn points by helping other students or get them with a premium plan

Guidelines and tips
Guidelines and tips
Sell on Docsity
Sell on Docsity
Docsity AI
Docsity AI
Log inSign up

Prepare for your exams

Study with the several resources on Docsity

Find documents

Prepare for your exams with the study notes shared by other students like you on Docsity

Search for your university

Find the specific documents for your university's exams

Docsity AINEW

Summarize your documents, ask them questions, convert them into quizzes and concept maps

Explore questions

Clear up your doubts by reading the answers to questions asked by your fellow students

Earn points to download

Earn points by helping other students or get them with a premium plan

Share documents
download point icon20 Points

For each uploaded document

Answer questions
download point icon5 Points

For each given answer (max 1 per day)

All the ways to get free points
Get points immediately

Choose a premium plan with all the points you need

Study Opportunities

Choose your next study program

Get in touch with the best universities in the world. Search through thousands of universities and official partners

Community

Ask the community

Ask the community for help and clear up your study doubts

Free resources

Our save-the-student-ebooks!

Download our free guides on studying techniques, anxiety management strategies, and thesis advice from Docsity tutors

Extracellular Matrix and Cell Junctions, Exams of Biology

Chamberlain College of NursingBiology

A comprehensive overview of the extracellular matrix (ecm) and cell junctions, which are crucial components of tissue structure and function. It covers the two main forms of the ecm, collagen, and the different types of cell junctions, including tight junctions, adherens junctions, desmosomes, and gap junctions. The document also discusses the role of cell adhesion molecules (cams) like cadherins and integrins in mediating cell-cell and cell-matrix interactions, as well as the importance of these interactions in processes like tissue organization, cell migration, and cancer metastasis. Additionally, the document touches on the structure and function of the basal lamina, a specialized form of the ecm that underlies epithelial cells. Overall, this document provides a detailed and comprehensive understanding of the extracellular matrix and cell junctions, which are fundamental to the study of cell biology, tissue engineering, and cancer biology.

Typology: Exams

2023/2024

Available from 08/09/2024

TheHub
TheHub šŸ‡ŗšŸ‡ø

3.9

(33)

11K documents

1 / 13

Toggle sidebar

This page cannot be seen from the preview

Don't miss anything!

bg1
PSU BMB 252 EXAM 3 QUESTIONS AND
ANSWERS 2024/2025
ECM
Extracellular matrix
a network of proteins and polysaccharide chains that are secreted by cells
two forms of the ECM
ECM of connective tissue= fibrous polymers like collagen
Basal Lamina= flexible, thin mat of specialized ECM that underlies epithelial cell sheets and tubes
Collagen
structural protein found in the skin and connective tissue- fibrous protein gives skin strength
two ways that cells are attached in tissue
either to the basal lamina or to the ECM and to each other
Basal Lamina
thin extracellular layer that lies underneath epithelial cells and separates them from other tissues
Epithelial Cells
skin cells that cover the outside of the body and line the internal surfaces of organs
4 main types of junctions
1. Tight junction
2. Cell-cell anchoring junction (adherens and desmosomes)
3. Gap junction
4. Cell-matrix anchoring junction (hemidesmosome and actin-linked cell-matrix junction)
Tight Junction
A type of intercellular junction in animal cells that prevents the leakage of material between cells.
adherins
cell junction used when you want to resist separation of cell membrane to anchor cells together using
microfilament (actin) and cadherin
desmosomes
Anchoring junctions that prevent cells from being pulled apart
gap junction
A type of intercellular junction in animals that allows the passage of materials between cells.
cell-matrix anchoring junction
connect cell to ECM
pf3
pf4
pf5
pf8
pf9
pfa
pfd

Partial preview of the text

Download Extracellular Matrix and Cell Junctions and more Exams Biology in PDF only on Docsity!

PSU BMB 252 EXAM 3 QUESTIONS AND

ANSWERS 2024/

ECM

Extracellular matrix a network of proteins and polysaccharide chains that are secreted by cells two forms of the ECM ECM of connective tissue= fibrous polymers like collagen Basal Lamina= flexible, thin mat of specialized ECM that underlies epithelial cell sheets and tubes Collagen structural protein found in the skin and connective tissue- fibrous protein gives skin strength two ways that cells are attached in tissue either to the basal lamina or to the ECM and to each other Basal Lamina thin extracellular layer that lies underneath epithelial cells and separates them from other tissues Epithelial Cells skin cells that cover the outside of the body and line the internal surfaces of organs 4 main types of junctions

  1. Tight junction
  2. Cell-cell anchoring junction (adherens and desmosomes)
  3. Gap junction
  4. Cell-matrix anchoring junction (hemidesmosome and actin-linked cell-matrix junction) Tight Junction A type of intercellular junction in animal cells that prevents the leakage of material between cells. adherins cell junction used when you want to resist separation of cell membrane to anchor cells together using microfilament (actin) and cadherin desmosomes Anchoring junctions that prevent cells from being pulled apart gap junction A type of intercellular junction in animals that allows the passage of materials between cells. cell-matrix anchoring junction connect cell to ECM

hemidesmosome anchors intermediate filaments in a cell to extracellular matrix intermediate filaments A component of the cytoskeleton that includes all filaments intermediate in size between microtubules and microfilaments Cadherins

  • anchoring junction that links cells together
  • transmembrane protein
  • depend on Ca cadherens = ca2+ + adherins Integrins anchoring junction that links cells to the ECM adherins junctions cell-cell anchoring junction that links actin filaments Desmosomes cell-cell anchoring junction that links intermediate filaments filament that forms a layer close to the cell surface actin actin A globular protein that links into chains, two of which twist helically about each other, forming microfilaments in muscle and other contractile elements in cells. the two cell-matrix anchoring junctions actin-linked cell-matrix adhesions (focal adhesions) and hemidesmosomes focal adhesions link actin filaments to the ECM Hemidesmosomes Link intermediate filaments to the ECM two types of cadherins classical= named according to tissue they were first found non-classical- more than 50 alone in brain N-cadherin P-cadherin E-cadherin N-cadherin --> nerve P-cadherin--> placenta, epidermis E-cadherin---> epithelial difference between homophilic and heterophilic binding
  • provide a permeability barrier
  • prevent the mixing of plasma membrane components type of transport that transports through epithelium cells transcellular transport epithelium cells form the lining of structures type of transport that is through tight junctions paracellular transport; passive transport that depends on concentration and there is no ATP used forms tight junctions claudins and occludins Claudins and occludins interact through _____ interactions homophilic claudin The major adhesion protein located in tight junctions occludin Regulatory protein that alters paracellular permeability. Stabilizes Tight junction What are ZO (zonula occludins)? proteins that serve as a scaffold type of pores that claudins form form paracellular pores that allow specific ions to pass gap junctions allow cell communication and are channels between cells that allow molecules < 1000 Da to pass How many g/mol is 1 Da? 1 Da = 1 g/mol Can a 3 kg/mol molecule pass through a gap junction? no Connexins form gap junctions How many connexins make up a connexon? 6 CAMs cell adhesion molecules selectins a CAM that binds to oligosaccharides on other cells (cell-cell adhesion) through heterophilic binding involved in immune responses Selectins are ___ dependent Ca

domain on selectin that binds to the oligosaccharide lectin domain oligosaccharide A carbohydrate made up of 3-10 sugar residues Participate in cell recognition and adhesionleu What cells do these selectins belong in?

**1. L-selectin

  1. P-selectin
  2. E-selectin**
  3. leukocytes
  4. platelets
  5. endothelial cells Leukocytes white blood cells, fight infection platelets blood clotting endothelial cells cells lining the blood vessels makes white blood cells roll along blood vessel walls selectins Ig-like CAMs type of CAM that is not Ca dependent and interacts through heterophilic and homophilic interactions cell adhesion three forms of the ECM bones and teeth transparent cornea tendons ECM is secreted from cells of fibroblast family GAGs long unbranched polysaccharides containing a repeating disaccharide unit hyaluronan a GAG that is a component of joint fluid proteoglycans polysaccharide GAG linked to protein (serine amino acid) Proteoglycans can form aggregates

scaffold pulling force at integrins talin unfolds revealing the vinculin binding site that results in the recruitment of more actin events that happen within a tumor

  1. mutation
  2. uncontrollable division
  3. connections between cells is lost
  4. natural selection laws rule the cells
  5. cells get more mutations and invade other tissues two stages of cancer development
  6. cells divide uncontrollably, giving rise to a tumor - neoplasm
  7. cells get ability to invade surrounding tissue and form secondary tumors - metastases metastasis cancer cells leaving a tumor and invading other parts of the body noninvasive tumor non-cancerous/ benign metastasizing tumor malignant, cancerous Cancers are called according to tissue or cell type Where are each of these cancers located? carcinoma sarcoma leukemia
  8. epithelial cells
  9. muscle or connective tissue
  10. hemopoietic cells doubling time for cancer 100 days evidence that cancers are derived from a single mutated cell
  11. chromosomal translocation analyses (in a person with cancer, all the cancer cells have the same translocation, but in cancer cells of two different people, patients have different translocations)
  12. X-chromosome inactivation analyses in female tumor cells (female tissues are a mixture of active and inactive x-chromosomes Hhiladelphia chromosome translocation happens at the exact same position in all patients False three changes that causes cancer
  1. genetic gene inactivation
  2. epigenetic gene inactivation with formation of heterochromatin
  3. epigenetic gene inactivation with methylation causes carcinogenesis (generation of cancer) mutagens and genetic predisposition a single mutation can cause cancer false The evolution of a tumor involves many rounds of ______ and ______ mutation and natural selection rate of evolution in cancer depends on
  4. mutation rate
  5. number of individuals
  6. rate of reproduction
  7. selective advantage of mutants over the normal cancers are unstable instability can result from defect in DNA repair and inability to maintain chromosome integrity ways to increase tumorigenesis increase cell division (take away cell division controls) and decrease apopotosis Cells survive only if they get survival signals or proliferation signals selective advantage that cancer cells have over normal cells telomeres do not shorten so they can divide unlimited number of times key aspects of cancerous cells
  • disregard external and internal signals regulating cell proliferation
  • avoid apoptosis
  • genetically unstable
  • invasive
  • metastatic
  • able to recruit adequate blood supply cancer-critical genes those genes that are altered frequently in human cancers The most common mutations are ______ and the rare ones are ______ drivers and passengers two categories of cancer critical genes oncogenes and tumor suppressor genes

first oncogene to be identified Oncogene Ras method of identifying oncogenes

  1. DNA extracted from tumor cells
  2. broken into fragments
  3. each fragment put in mouse-derived cells line which has cancer mutations
  4. if fragment has oncogenes, then small colonies form
  5. sequence the fragment and find the oncogene ways that proto-oncogenes convert to oncogenes
  6. hyperactive protein
  7. elevate protein by gene amplification
  8. chromosomal rearrangement that hyperactives expression of gene How the myc proto-oncogene turns into an oncogene amplification What is Ras? What happens when its mutated? a GTpase that helps to transmit the signal to enter the cell cycle. When there is a mutation, it leads to cancer because the signal is transmitted without any signal What is Myc? What happens when it is mutated? Myc is a gene regulatory protein that promotes cell division. When there is a mutation, the overproduction causes cancer. two tumor suppressor proteins we learned p53 and Rb identify a tumor suppressor by finding something that is missing in the cancer cell Rb acts in a _____ manner recessive _____ copies of Rb should be lost to cause cancer Both What does phosphorylation of Rb do? What phosphorylates it? Phosphorylation of Rb by cyclin/CDK relives inhibition of E2F and allows it to activate transcription of S- phase genes Phosphorylating Rb renders it inactive what it looks like in a non-proliferating cell with Rb In a non-proliferating cell, cyclin/CDK is inactive by p16 and active Rb is bound to E2F to stop the expression of S-phase genes main tumor suppressor gene p

functions of p

  • plays a role in apoptosis, genomic stability, and inhibition of angiogenesis
  • activates DNA repair proteins
  • arrests cell in G1/S checkpoint so proteins can fix DNA
  • initiates apoptosis if needed loss in p53 results in aneuploidy phenotype increased amount of p53 causes increased aging cell cycle arrest pathway with p53 in response to DNA damage
  1. DNA is damaged
  2. protein kinases become active
  3. protein kinases phosphorylate p53 to make it active
  4. p53 binds to regulatory region of p21 gene
  5. p21 mRNA made, then p21 protein (which is a Cdk inhibitor protein)
  6. p21 binds to G1/S-Cdk and S-Cdk to arrest cell in G1 phase so other proteins can fix the damaged DNA structural aspects of p Has DNA-binding domain, has domains for apoptotic activity, has transcription activation domain Mutations in which domain of p53 require both alleles to be mutated in order to cause cancer (recessive loss of function mutations) DNA binding domain (recessive loss-of-function mutation) mutations in oligomerization domains in p prevent the formation of tetramers for transcription activation (dominant negative effect on p53 function) most commonly mutated gene in colorectal cancer APC gene Smad transcription factor that is activated by TGF-beta signaling molecule happens when Smad4 is mutated cells proliferate uncontrollably Wnt/B-catenin signaling pathway Without Wnt signal:
  • frizzled GPCR not bound with Wnt signal
  • B-catenin is unstable
  • there is block on transcription regulator that causes the Wnt genes to not be transcribed and are off With Wnt signal:

polymerase involved in DNA repair happens to cancer cells with the inhibition of PARP inability to seal single stranded breaks and so cancer cells die cells that ionizing radiation kills cancer cells and some normal cells cells that mostly die by apoptosis normal cells causes CML (associated with philadelphia chromosome) fusion kinase that is active without the signal Gleevec inhibits fusion Abl and normal Abl Cancers inhibit immune system cells by Binding to inhibitory receptors plays a role in breast cancer risk When a women had her first child PARP becomes inactive cancer cells can restore BRCA proteins by other mutations an approach to overcome drug resistance with cancer cells Combination therapies where you treat with multiple treatments and not one at a time