I am stuck on a question about cell growth signaling and RTKs. If phosphatase is nonfunctional, could it lead to uncontrollable growth resulting in cancer?
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I am stuck on a question about cell growth signaling and RTKs.
If phosphatase is nonfunctional, could it lead to uncontrollable growth resulting in cancer?
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- Can I get help please with this question? Two mutations have occurred to proteins within the glucagon signaling pathway: A) The glucagon receptor has a mutation. This mutation causes this GPCR to always have a conformation that will induce nucleotide exchange for any associated heterotrimeric G proteins, even without glucagon binding to the receptor. B) The alpha subunit of the heterotrimeric G protein has a mutation. This mutation causes the Gαarginine finger to always be in a position to properly order the catalytic residues within the Gαsubunit to promote catalysis. Question: What will the combined effect of both mutations be on the signaling pathway and what is the mechanistic reason for this effect?"given the numerous processes inside cells that are regulated by changes in Ca+2 concentration, it seems likely that Ca¹²-dependent cell-cell adhesions are also regulated by changes in Ca2 concentration" is true or false.Figure 9.8 HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is permanently activated, resulting in unregulated cell division. Lapatinib, a drug used to treat breast cancer, inhibits HER2 receptor tyrosine kinase autophosphorylation (the process by which the receptor adds phosphates onto itself), thus reducing tumor growth by 50 percent. Besides autophosphorylation, which of the following steps would be inhibited by Lapatinib? Signaling molecule binding, dimerization, and the downstream cellular response. Dimerization, and the downstream cellular response. The downstream cellular response. Phosphatase activity, dimerization, and the downsteam cellular response.
- Certain types of cancerous lung tumors can secrete hormones normally made by the pancreas, adrenal gland, and hypothalamus. What prevents such secretion of happening in healthy cells?I just read an abstract of the paper “Disulfide bond-disrupting agents activate the tumor necrosis family-related apoptosis-inducing ligand/death receptor 5 pathway” and noted that “DDAs and TRAIL synergize to kill cancer cells and are cytotoxic to HER2+ cancer cells with acquired resistance to the EGFR/HER2 tyrosine kinase inhibitor Lapatinib.” For the last sentence, I am not sure the meaning of the “acquired resistance to the EGFR/HER2 tyrosine kinase inhibitor Lapatinib”. Is the “acquired resistance ... to inhibitor” a good thing or bad thing, as far as the synergize effect of DDAs and TRAIL”? Hope that expert can help.This question pertains to membrane transport and cell signaling. What are kinases and phosphatases? Why are they important in cellular signaling pathways?
- My question is two fold. What are some diseases that cause and/or are caused by apoptosis? Also if apoptosis is the most common form of programmed cell death in animals, what other forms of programmed cell death are there? Thank you.Many malignant tumors are characterized by the activation of one or more growth-factor receptors. What is the catalytic activity associated with transmembrane growth factor receptors such as the EGF receptor?What is the relationship between Warburg effect and oncogenesis? Explain why cancer cells have inefficient ATP production.
- MPF plays an important role during the regulation of the cell cycle. give examples that will support this statement.Artificially induced apoptosis (controlled cellular death) is found to be an effective treat- ment for some forms of cancer. Which of the following describes the most likely mechanism by which apoptosis might be induced? A B с D by causing ribosomes to increase the rate of protein synthesis by triggering the division of mitochondria in the cell to increase ATP production by increasing the expression of membrane-bound glucose protein channels by causing lysosomes to release digestive enzymes into the cytosolWhat is the main benefit of cell signaling over long distances (ex: signaling via hormone secretion into the bloodstream)?