Notch signaling orchestrates transition from G1 to S phase of cell cycle by multiple other interactions that target the G1/S checkpoint machinery. This is a highly conserved pathway that is seen across multiple kingdoms of life and the ligands involved in notch signaling are typically membrane-bound proteins. This suggests that: -This pathway relies on hormone interactions via endocrine pathways -This pathway relies on signal propagation via paracrine molecules -This pathway relies on direct signaling across gap junctions -This pathway relies on cell binding via autocrine signaling

Notch signaling orchestrates transition from G1 to S phase of cell cycle by multiple other interactions that target the G1/S checkpoint machinery. This is a highly conserved pathway that is seen across multiple kingdoms of life and the ligands involved in notch signaling are typically membrane-bound proteins. This suggests that: -This pathway relies on hormone interactions via endocrine pathways -This pathway relies on signal propagation via paracrine molecules -This pathway relies on direct signaling across gap junctions -This pathway relies on cell binding via autocrine signaling

Biology 2e

2nd Edition

ISBN:9781947172517

Author:Matthew Douglas, Jung Choi, Mary Ann Clark

Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark

Chapter9: Cell Communication

Section: Chapter Questions

Problem 1VCQ: Figure 9.8 HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is...

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In response to a hormone secreted by a cell of the opposite mating type, a yeast cell undergoes a complex series of physiological changes involving the activity of about 200 genes and cytoplasmic proteins. They include blockingDNA synthesis, growing toward the mating partner, fusion of the plasma membranes of the two cells, and fusion of their nuclear membranes. Explain how all these events can be controlled through a complex signaling cascade that is triggered by the binding of the hormone to a G protein–linkedreceptor.
This phosphatase removes an inhibitory phosphotyrosine phosphate from serine protein kinase, mentioned in question 6, which activates kinase. What phosphatase is it? This is what question 6 says....This is the serine protein kinase that when activated in a complex cyclin, controls onset of mitosis and M-phase of the cell cycle. 1. Cyclin A/B 2. Wee 1 3. TOR (Target of Rapmycin) 4. Cdk1 5. none of the these ***I believe the answer is Cdk1 for number 6, but I could be wrong
What is the effect of having fluctuating cyclin levels throughout the cell cycle, while the levels of its corresponding cyclin dependent kinase stay relatively constant? Explain.
Which of the following is the primary method by which cyclin proteins are regulated to influence entry into the cell cycle or transition from one stage to the next? A. Transcriptional upregulation and translation followed by targeted ubiquitin-mediated degradation by a proteasome. B. Phosphorylation to regulate the activity of the kinase site. C. An activating phosphorylation and an inactivating phosphorylation. D. All of these are mechanisms that can be used to regulate cyclins.
Regulation of the cell cycle is very complex and involves multiple proteins. In yeast, a complex of cdc2 and a mitotic cyclin is responsible for moving the cell past the G2/M checkpoint. The activity of the cyclin-dependent kinase cdc2 is inhibited when it is phosphorylated by the kinase, Wee-1. What would you predict would be the phenotype of a Wee-1 mutant yeast? What other genes could be altered in a Wee-1 deficient mutant strain that would make the cells act normally?
a. A typical cellular response of a mammary epithelial cell to EGF signal is proliferation. the Kd for the interaction between EGF and its receptor is 1x10^-10 M. Lets imagine that at least 25% of the receptors on a normal cell must be engaged by EGD in order to trigger the cellular proliferation response. What minimum concentration of EGF is required to reduce cell proliferation? (Show calculation). b. Mammary epithelial cancer cells have amplified levels of EGF receptors on their surface. If such a cell has 1000 EGF receptors, as compared to 200 receptors on a normal cell, what minimum concentration of EGF is required to induce cell proliferation in the cancer cell? [Show calculation]. Note that the same number of receptors (not percentage of receptors) must be activated to promote proliferation in normal cells and cancer cell. c. The ambient (unstimulated) concentration of EGF in mammary epithelial tissue is 1x10^-11 M. Will this level of EGF stimulate proliferation in normal…
Which of the following statements is a lie?Select one: a. If damaged DNA is detected during the cell cycle, negative regulation is responsible in stopping the cell cycle. b. There are four cyclin proteins involved in the positive regulation of the cell cycle and they have fluctuating levels. c. To activate cyclin-dependent kinases (Cdks), they must bind to another kinase.
Insulin-like growth factor (IGF) is a peptide hormone (ligand) that binds and activates IGF receptor tyrosine kinase. Once the ligands bind the receptors, the cell undergoes cell division and multiply. Therefore, IGF is important for the growth of muscle and bone tissues during puberty. The way the IGF hormone works is that the hormone-bound IGF receptor tyrosine kinase increases the levels of cyclins inside of the cell and promotes the progression of the cell cycle. Describe how receptor tyrosine kinase works in a general sense and how cyclins regulate the cell cycle.
Below are two cell signalling pathways that work together to regulate cell growth, proliferation and ultimately the size of organs in O.Extremus. In other closely related organisms, dysfunction of these pathways has been associated with tumor growth. mTOR pathway: 1. Growth factors bind and stimulate the receptors. 2. Receptors can activate the phosphatidylinositol 3 kinase (PI3K) – Akt signaling pathway. 3. The activated Akt, a serine threonine kinase, inhibits theTSC1–TSC2 complex, allowing Rheb to activate mTORC1. 4. In parallel, amino acids activate the mTORC1 pathway through a mechanism requiring the Rag– Ragulator complex. Hippo pathway: 1. The binding of the ligand activates the receptors which activate Mst and Lats. 2. YAP activity is modulated by phosphorylation of Mst and Lats. YAP upregulates miR-29, which in turn downregulates PTEN, an inhibitor of PI(3)K and Akt. So, the two pathways crosstalk and coordinate cell number and growth. a) What purpose does this forward…
Maturation promoting factor, MPF, is a cyclin-CDK complex that catalyzes the phosphorylation of other proteins to start mitosis. The activity level of MPF is dependent on the relative concentrations of the cyclin and CDK components of MPF (Figure 1). Based on Figure 1, which of the following describes the role of cyclin in the regulation of the cell cycle? a.During S phase, the cyclin level remains the same because DNA replication is occurring. b.During G2 phase, the cyclin level remains low, causing MPF activity to decrease, which leads cells to initiate mitosis. c.During G1 phase, the cyclin level decreases to signal the start of the resting phase of the cell cycle. d.During M phase, the cyclin level peaks, resulting in an increased binding frequency with CDK.
The expression of this inhibitor of G2 to M Phase of the cell cycle progression will be significantly upregulated in a muscle cell that has had a drastic drop in insulin stimulation due to glucose and amino acids withdrawal; Group of answer choices ARF CiP/KiP-p21 CiP/KiP-p27 p57
Cell lines divide normally in a defined medium containing growth factors, but fail to divide in the absence AGF (a growth factor). However, a mutant cell line continues to divide even in the absence of AGF. Elevated levels of Rb phosphorylation and the effects of receptor and Mek inhibitors suggest a mutation activating an oncogene. Inhibitors of Mek inhibit cell division of the mutant cell line, but inhibitors to the ADGF receptor, a receptor tyrosine kinase (RTK) with homology to EGFR, do not. Outline the RTK pathway leading to the phosphorylation of Rb to form p-Rb.