Cell Cycle Control and Regulation

• Before a cell enters M phase, centrosomes and chromosomes must undergo duplication.
• Cell growth predominantly occurs during the G2 phase of the cell cycle.
• The time to complete a cell cycle varies among eukaryotic cells, with stage variations depending on cell type; for example, rapidly dividing embryonic cells may eliminate the G1 phase.
• Adding colchicine at the metaphase-anaphase transition results in chromosome segregation without cell elongation due to microtubule disruption.
• Mitotic Cdk is present throughout all cell cycle phases, whereas cyclin concentrations fluctuate.
• Fusing early G1 phase cells with S-phase cells triggers DNA replication in the G1 cells.
• Generation time is the time it takes a cell to complete one cell cycle.
• Kinetochores assemble on chromosome centromeres during late prophase, and kinetochore microtubules attach to kinetochores.
• Cyclin binding to Cdk is essential for Cdk's enzymatic activity, enabling cell cycle progression.
• Under-expression of Mad or Bub proteins can lead to premature APC activation, causing chromatid separation and potential non-disjunction.
• At metaphase, sister chromatids are actively pulled toward opposite poles, despite the appearance of inactivity.
• Microtubule motor proteins function during mitosis to shorten kinetochore microtubules, pull them in at centrosomes, push interpolar microtubules for anaphase, and pull astral microtubules toward the cell cortex.
• A cell lacking a G2 checkpoint protein will enter M phase inappropriately.
• Cyclins regulate cell cycle progression by activating protein kinases.
• Cdk activity changes due to fluctuating cyclin levels, not Cdk synthesis or degradation.
• If the Rb protein cannot be phosphorylated, the cell will not enter S phase.
• The G2-M checkpoint assesses DNA replication status.
• Mitotic Cdk-cyclin is active when singly phosphorylated.
• The anaphase-promoting complex (APC) is not continuously active throughout the cell cycle.
• Mitotic cyclin (M cyclin) concentration decreases due to ubiquitylation and degradation at the end of M phase.
• Phosphorylation of condensin is essential for chromosome condensation.
• Cohesins hold sister chromatids together after DNA replication.
• Microtubule depolymerization during mitosis prevents chromosome alignment in metaphase.
• The Retinoblastoma (Rb) protein inhibits cyclin transcription, blocking cell entry into the cell cycle.
• The G1 DNA damage checkpoint inhibits cyclin–Cdk complexes via p21.
• The relationship of Raf to MEK mirrors that of MEK to MAPK.
• Rho proteins regulate the assembly and activation of the contractile ring for cytokinesis.
• CENP-A is not involved in DNA replication licensing during S phase.
• The PI3-kinase activation pathway for cell division proceeds as: PIP3 formation, Akt phosphorylation, and TOR activation.
• Irradiated mammalian cells halt at the G1 checkpoint in the order: DNA damage, p53 accumulation and activation, p21 production, and cyclin–Cdk complex inhibition.
• Cytotoxic lymphocytes can trigger self-destruction in target cells via Death Receptor interaction.
• Apoptosis involves caspases, death signals, mitochondria, and Bcl-2, but not APC ubiquitin ligase activity.
• Apoptosis is involved in digit webbing removal, neuron reduction during brain development, pathogen-infected cell destruction, and white blood cell removal at life's end, but not cancer tumor generation.
• Necrosis involves cell rupture, unlike apoptosis.
• Apoptosis is promoted by cytochrome c release from mitochondria into the cytosol.

Protein Roles

• Bcl-2 is involved in apoptosis.
• p53 directly regulates cell cycle processes.
• Ras is involved in mitogen signaling pathways.
• Securin is important for chromosome separation and cytokinesis.
• APC is also involved in chromosome separation and cytokinesis.
• MAPK is a component of mitogen signaling pathways.
• Cdk directly regulates cell cycle processes.
• Cytochrome c promotes apoptosis.
• Hormones are suited for sending signals to most cells throughout a multicellular organism.
• Regulation of inflammatory responses at an infection site is an example of paracrine signaling.
• Kinases and phosphatases turn proteins "on and off" via phosphorylation status.
• Hydrophilic extracellular signal molecules require cell-surface receptors to signal target cells.
• Protein kinases transfer a terminal phosphate from ATP to a protein; serine/threonine kinases are common types of protein kinases; GTP-binding proteins exchange GDP for GTP to activate and a GAP is used instead of a phosphatase to help the molecular switch to hydrolyze GTP.
• G-protein-coupled receptors activate G proteins, causing the α subunit to exchange GDP for GTP.
• The duration of G protein signaling is determined by the GTPase activity of Gα.

G Protein Targets and Outcomes

• Adenylyl cyclase leads to increased cAMP levels.
• Ion channels lead to changes in membrane potential.
• Phospholipase C leads to cleavage of inositol phospholipids.
• The steps in the EGF–cAMP signaling pathway are: ligand binding, G-protein activation, adenylyl cyclase activation, cAMP production, and protein kinase A activation.
• cAMP interacts directly with protein kinase A regulatory subunits.
• IP3 receptors, associated with ER membranes, aid in calcium release.
• A protein kinase acts as an integrating device if activated by proteins in different signaling pathways.
• Dephosphorylation by serine/threonine phosphatases is not directly involved in inactivating an activated RTK.
• Ras does not bind steroid hormones.
• Akt promotes cell survival by affecting Bad and Bcl2; in the absence of a survival signal, Bad is not phosphorylated.
• Autophosphorylation in receptor tyrosine kinases provides recruitment sites for signal transduction molecules.
• If Ras GTPase activity is abolished, MAP kinases are continuously activated, promoting continuous mitotic divisions.
• Terminally differentiated cells can no longer divide.
• Terminally differentiated cells are replaced by proliferating precursor cells.
• A stem cell divides into a terminally differentiated cell and a stem cell.
• Malignant tumors are more dangerous due to their ability to invade other tissues.
• A mutation introducing a stop codon after the initiator methionine cannot convert a proto-oncogene into an oncogene.
• Growth in liquid medium is an immediate consequence of anchorage-independent cancer cell growth.
• Alterations that could cause increased cell proliferation include an alteration of a protein that normally promotes apoptosis and alteration of a protein that normally prevents progress through the cell cycle if there is something defective about the cell.
• Tumor suppressor gene absence promotes cancer, while oncogene presence promotes cancer.
• Cells with one functional copy of a tumor suppressor gene usually do not proliferate faster than normal cells.
• Density-dependent inhibition of growth does not contribute to cancer cell proliferation.
• Cancer cells generally divide at the same rate as normal cells.
• Oncogene expression contributes to cancer development.
• Cancer cell aneuploidy is likely caused by a Mad defect.
• Histone methylation is not a mechanism by which proto-oncogenes are converted to oncogenes.
• Hereditary breast and ovarian cancer often arises from a mutant copy of BRCA1 or BRCA2, involved in DNA double-strand break repair.
• A physician would not expect to find perfectly spherical nuclei when examining suspect cells in biopsy tissue
• Cancer screening procedures include pap smears, mammography, Sept 9 expression levels, and colonoscopies.