Cell Bio - Exam 4 slide Flashcards

G1 Phase

First Growth Phase of interphase where the cell grows and prepares for DNA synthesis

S Phase

Synthesis Phase of interphase where DNA replication occurs

G2 Phase

Second Growth Phase of interphase where the cell undergoes further growth and prepares for mitosis

G0 Phase

Zero Growth Phase where the cell exits the cell cycle and becomes quiescent

M Phase

Phase of the cell cycle consisting of mitosis (division of the nucleus) and cytokinesis (division of the cytoplasm)

Restriction Point

Key checkpoint at the G1/S transition where the cell commits to division or exits to G0

Cyclin-Dependent Kinases (CDKs)

Kinases that are activated by binding to cyclins and phosphorylate tumor suppressor proteins to deactivate them, allowing progression through the cell cycle

Cyclin D + CDK4/6

Complex active in early G1 that partially phosphorylates Rb protein

Cyclin E + CDK2

Complex active at G1/S transition (restriction point) that fully phosphorylates Rb and p27, and forms DNA prereplication complexes

Cyclin A + CDK2/1

Complex active in S phase that phosphorylates E2F and replaces cyclin E to prevent new pre-replication complexes

Cyclin B + CDK1

Complex active at G2/M transition that triggers mitosis and is degraded after the metaphase-anaphase transition

Rb (Retinoblastoma protein)

Tumor suppressor protein that normally binds transcription factor E2F to block it; when phosphorylated by CDKs, it releases E2F

E2F

Transcription factor that is normally bound by Rb; when released by Rb phosphorylation, it activates genes for S phase including cyclins E and A

G1/S Restriction Point Checkpoint

Checkpoint that checks for sufficient cell size and nutrients; failure activates cyclin kinase inhibitors (CKIs) to hold the cell in G1 or G0

End of G2 Checkpoint

Checkpoint that checks for DNA damage via ATR, ATM, and DNA-PK; attempts repair using parent strand as template or triggers apoptosis if irreparable

Metaphase Checkpoint (Spindle Checkpoint)

Checkpoint that checks for tension on kinetochores (equal pulling from both poles); failure triggers apoptosis

Two-Hit Hypothesis

Theory that most tumor suppressor genes are dominant and both alleles must be lost for cancer to develop

Multimodal Hypothesis

Theory that cancer requires at least ONE gain-of-function mutation in proto-oncogenes AND at least ONE loss-of-function mutation in tumor suppressor genes

p53

Transcription factor known as "guardian of the genome" that is activated by ATR/ATM in response to DNA damage and activates p21

p21

Protein that inhibits CDK2, CDK3, CDK4, and CDK6 to halt the cell cycle in response to DNA damage

Cadherins

Calcium-adhering Cell Adhesion Molecules that are homophilic (bind same type) and calcium ion sensitive; example is E-cadherin in epithelial cells

Selectins

Heterophilic Cell Adhesion Molecules that are calcium ion sensitive and bind carbohydrates

Integrins

Heterophilic Cell Adhesion Molecules that are calcium ion sensitive and bind Type III intermediate filaments

Immunoglobulin (Ig) Superfamily CAMs

Most diverse class of Cell Adhesion Molecules that can be homophilic or heterophilic and are calcium ion insensitive

Mechanotransduction

Process by which CAMs convert mechanical stimuli (stress, tension) into signaling pathways

Tight Junctions

Cell junctions that don't permit diffusion between cells, formed by occludin, claudin, and JAMs; maintain cell polarity and create barriers in epithelial tissues

Gap Junctions

Cell junctions that permit diffusion of cytosol between adjoining cells, formed by connexins, innexins, and pannexins; important for rapid communication in cardiac tissue

Adherens Junctions

Anchoring junctions composed of cadherin plus microfilaments (actin) that hold cells together

Desmosomes

Anchoring junctions composed of cadherin plus intermediate filaments that hold cells together

Hemidesmosomes

Anchoring junctions composed of integrin plus intermediate filaments that attach cells to the ECM

Basal Lamina

Layer of ECM closest to cells, composed of collagen IV, laminin, nidogen/entactin, and heparan sulfate-proteoglycans; acts as foundation for tissue growth

Interstitial Matrix

Loose network layer of ECM composed of polysaccharides (proteoglycans and hyaluronic acid) and proteins (collagen, elastin) that provide gel-like consistency and structural support

Epithelial-to-Mesenchymal Transition (EMT)

Process where cells switch from E-cadherin to N-cadherin, promoting migration; occurs in embryogenesis and is exploited by cancer cells for metastasis

E-cadherin

Epithelial cadherin that keeps cells together; downregulated in metastatic cancer

N-cadherin

Neuronal cadherin that promotes migration and activates Ras/MAP pathway to promote cell reproduction; upregulated in metastatic cancer

Totipotent

Highest level of stem cell potency from zygote until blastula formation; can become ANY cell type or germ layer

Pluripotent

Stem cell potency level from blastula through gastrula stage; can become ANY cell derived from its germ layer

Multipotent

Adult stem cell potency level after gastrula; can differentiate into limited cell types based on tissue location

Progenitor Cells

Partially differentiated cells with limited self-renewal capacity

Oct4 and Sox2

Master transcription factors in embryonic stem cells that activate genes for self-renewal and pluripotency

Nanog

Master transcription factor in embryonic stem cells that represses genes that induce differentiation

iPSCs (Induced Pluripotent Stem Cells)

Stem cells created from differentiated somatic cells using master transcription factors; can differentiate infinitely in strict growth conditions

Apoptosis

Programmed cell death by self-destruction and fragmentation into "bite-sized chunks" that are internalized in apoptotic bodies and engulfed by phagocytes

Necroptosis

Programmed cell death by self-destruction after damage detection; cell produces porins to lyse itself, usually triggered by extrinsic factors and leads to inflammation

Necrosis

Accidental cell death where damage occurs too quickly for cell response; cell leaks into ECM and is pro-inflammatory

Caspases

Proteases activated in mitochondria that execute apoptosis

Bad (BH3-only protein)

PI3 kinase pathway member that promotes caspase activity when dephosphorylated in the absence of trophic factors

SMAC/DIABLO

Proteins that inhibit apoptosis-inhibiting proteins and promote caspase activity

Phosphatidylserine

Phospholipid switched from cytosolic to extracellular side of membrane during apoptosis to serve as "eat me" signal to phagocytes

Mitophagy

Targeted destruction of mitochondria, occurs early in apoptosis and is activated by p53

RIPK (Receptor-Interacting Protein Kinase)

Protein kinase activated by death receptors during necroptosis that activates pores in mitochondria and plasma membrane

Single Nucleotide Polymorphisms (SNPs)

Type of mutation where a single nucleotide is substituted; often silent with no effect

Indels

Insertion or deletion of one or more nucleotides; frequently cause frameshifts

Copy Number Variations (CNV)

Variation in the number of repeats of a genetic sequence; can affect short tandem repeats or whole genes

Chromosome Translocation

Mutation where a chromosome breaks and part is relocated to another chromosome

Aneuploidy (Chromosome Nondisjunction)

Mutation where chromosome pairs fail to separate during cell division; can affect single chromosome or entire genome

Driver Mutations

Mutations that cause cancer; most commonly loss-of-function in tumor suppressor genes (p53, Rb, BRCA) or gain-of-function in cell proliferation genes (Ras, Myc)

Warburg Effect

Metabolic transformation in cancer cells where they switch from efficient oxidative phosphorylation to inefficient glycolysis/fermentation

Angiogenesis

Formation of new blood vessels; essential for cancer growth and provides highway for metastasis; stimulated by hypoxia-induced EPO release

Mitochondrial Parasitism

Process where cancer cells grow nanotubules to surrounding cells to siphon healthy mitochondria, weakening healthy tissue

Chemotherapy

Cancer treatment designed to inhibit cell function or kill through toxicity; examples include Taxol (prevents microtubule disassembly) and Temodar (methylates DNA)

CAR T Cell Therapy

Cancer treatment using Chimeric Antigen Receptor T cells engineered from patient's white blood cells to identify tumor-specific antigens

Monoclonal Antibodies

Lab-made antibodies that tag tumor-specific antigens to act as "eat me" signals to phagocytes and can interfere with protein function

Asymmetric Cell Division

Type of stem cell division where one daughter cell stays a stem cell and one differentiates due to uneven distribution of cellular contents

Trophic Factors

Growth factors whose presence prevents apoptosis by causing trophic receptors to phosphorylate BH3-only proteins like Bad, which inhibits caspases

Separase

Enzyme that cleaves cohesin to allow the metaphase to anaphase transition during mitosis

JAMs (Junctional Adhesion Molecules)

Proteins that form tight junctions along with occludin and claudin

Connexins

Proteins that create hemichannels to form gap junctions, along with innexins and pannexins

Laminin

Protein component of basal lamina; Type V intermediate filaments (lamins) provide strength

Dedifferentiation

Loss of specialized cell features; cancer cells are less differentiated than healthy cells and lose polarity, making them unable to perform specialized functions

Ubiquitination

Process of protein degradation that decreases cyclin concentration during cell cycle progression

ATR, ATM, DNA-PK

Proteins that detect DNA damage at the end of G2 checkpoint and activate p53 if damage is detected

Interphase

Majority of cell life consisting of G1, S, G2, and G0 phases

Mitosis

Division of the nucleus during M phase

Cytokinesis

Division of the cytoplasm during M phase

Cyclin concentration regulation

Cyclins decrease in concentration via ubiquitination (degradation) to control cell cycle progression

Rb and E2F mechanism

Rb normally binds E2F transcription factor to block it; CDK phosphorylation of Rb releases E2F, which then activates genes for S phase

DNA prereplication complexes

Structures formed by Cyclin E + CDK2 at the G1/S transition to prepare for DNA replication

Cyclin Kinase Inhibitors (CKIs)

Proteins activated when the G1/S checkpoint fails that hold the cell in G1 or G0

Retinoblastoma example

Cancer caused by Rb gene mutations leading to overexpression of G1/S cyclins and uncontrolled proliferation

Homophilic binding

Type of binding where CAMs bind to the same type of molecule (e.g., cadherins)

Heterophilic binding

Type of binding where CAMs bind to different types of molecules (e.g., selectins and integrins)

Type III intermediate filaments

Structural proteins that integrins bind to

Cell polarity

Structural organization of cells maintained by tight junctions; lost in cancer cells

Blood-brain barrier

Tissue with tight junctions creating an impermeable basal lamina

Intestinal lining

Tissue with tight junctions that create a barrier and maintain cell polarity

Cardiac tissue

Tissue where gap junctions are important for rapid communication and coordination

Smooth muscle coordination

Function requiring gap junctions for rapid communication between cells

Hemichannels

Structures created by connexins, innexins, and pannexins that form gap junctions

Collagen IV

Protein component of the basal lamina

Nidogen/Entactin

Protein component of the basal lamina

Heparan sulfate-proteoglycans

Component of the basal lamina

Lamins

Type V intermediate filaments that provide strength to the basal lamina

Kidney glomerulus

Tissue with highly permeable basal lamina

Proteoglycans

Polysaccharides in the interstitial matrix that provide gel-like consistency and attract water

Hyaluronic acid

Polysaccharide in the interstitial matrix that provides gel-like consistency and attracts water