Biochemistry
9th Edition
ISBN: 9781319114671
Author: Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.
Publisher: W. H. Freeman
expand_more
expand_more
format_list_bulleted
Concept explainers
Question
Herceptin is an antibody that is used to treat certain forms of breast cancer by binding to a class of estrogen receptors. What is the basis for its effectiveness in treating certain forms of breast cancer?
Expert Solution
This question has been solved!
Explore an expertly crafted, step-by-step solution for a thorough understanding of key concepts.
This is a popular solution
Trending nowThis is a popular solution!
Step by stepSolved in 2 steps
Knowledge Booster
Learn more about
Need a deep-dive on the concept behind this application? Look no further. Learn more about this topic, biochemistry and related others by exploring similar questions and additional content below.Similar questions
- To study the immune responses that provide protection against tumor growth in mice, some investigations have used the EL4 mouse thymoma line. This tumor cell line was derived from a C57BL/6 mouse, and represents a type of T cell lymphoma. When transplanted into Rag-deficient mice, the mice rapidly succumb to the tumor. This is also the case when the mice receive wild-type C57BL/6 T cells the day before tumor cell injection. However, Rag-deficient mice were protected when the transferred T cells came from mice that lacked expression of one cytokine receptor, as shown in the fugure below. Name one likely candidate for the cytokine receptor that is knocked out in the T cells that are able to protect the mice.arrow_forwardWhen T cells are activated by recognizing peptide:MHC complexes on dendritic cells in the lymph node, they up-regulate the receptor CD69. For T cells expressing a given T-cell receptor, the initial strength of the T-cell receptor signal can be modulated by varying the number of peptide:MHC complexes on the dendritic cells, or by varying the affinity with which the T cell-receptor binds to the peptide:MHC complexes. As a result, T cells stimulated with stronger T-cell receptor signals will maintain high expression of CD69 for one or two days longer that if those same T cells were stimulated with weaker T-cell receptor signals. Therefore, T cells stimulated with weaker T-cell receptor signals are likely to: Die by apoptosis Undergo more rounds of proliferation that T cells stimulated with stronger T-cell receptor signals Migrate to the B-cell zones of the lymph node Have reduced effector functions, such as cytokine production Egress from the lymph node 1–2 days earlier than T cells…arrow_forwardWhich proteins involved in the activation of T cells have the capacity for transduction without the need to be activated by a family of kinases?arrow_forward
- Please give the answers onlyarrow_forwardSort the following steps of GPCR signal propagation (you may not use all the steps): A) Dephosphorylation of GPCR B) G protein dissociation to adenylate cyclase and GTP binds to the G protein C) Ligand binding to GPCR D) G protein dissociation from GPCR and GDP binds to the G protein E) Synthesis of CAMP F) Activation of PKA G) G protein association to adenylate cyclase H) G protein dissociation from GPCR and GTP binds to the G protein O F, C, H, F, B OC OB, D, A, E, H O C, H, G, E, F OA, G, H, B, Earrow_forwardYou are in the process of developing a monoclonal antibody against an Influenza virus spike protein "H7." You have isolated the B cells producing antibodies against the viral H7 protein and fused those specific B cells with a unique kind of mutant myeloma cells. The myeloma cells can't make any of the three following enzymes; dihydrofolate reductase (DHFR), thymidine kinase (TK), and hypoxanthine-guanosine phosphoribosyl transferase (HGPRT). The mutant unfused myeloma cells are grown in the laboratory in a nucleotide supplemented medium. For selecting the hybridomas, you have used a modified medium HT that does not contain any aminopterin but contains hypoxanthine and thymidine. Which of the following result do you expect to see from your experiment, and what problem you may encounter in the future after the hybridoma selection?arrow_forward
- Please outline the general steps you would take to test your hypothesis that SIN-47 works by disrupting the interaction between LEK2 and JAK4, You have: -several dishes of cancer cells -antibodies to LEK2 and JAK 4 -lots of the SIN-47 drugarrow_forwardWhich of the following drugs is a clinically-used monoclonal antibody for the treatment of breast cancer? O a. Doxycycline O b. Chloroquine O c. Herceptin O d. Protiumarrow_forwardHow do T cells, NK cells and macrophages recognize and destroy cells? How do cancer cells protect themselves from these cells? Explain how monoclonal antibodies and CAR-T-cells are used in cancer therapy. What are the advantages of these therapies?arrow_forward
- What are synthetic cannabinoids? where did they come from and what are their effects?arrow_forwarddescribe how the cellular response to EGF results in tissue repair (epidermal growth factor)arrow_forwardThe production of antimicrobial peptides is one of the most evolutionarily ancient mechanisms of defense for multicellular organisms, and most eukaryotic species make many different forms of these proteins. For instance, human paneth cells in the gastrointestinal epithelium make 21 different defensins. The reason for this diversity of antimicrobial peptides is: Epithelial cells make different forms than those made by neutrophils. Neutrophils make many different defensins and store them as inactive proteins in their secretory granules. Most of them are produced only in response to infection. The production of different peptides is induced following a bacterial infection versus a fungal infection. Each one has distinct activities against Gram-negative bacteria, Gram-positive bacteria, or fungi.arrow_forward
arrow_back_ios
SEE MORE QUESTIONS
arrow_forward_ios
Recommended textbooks for you
- BiochemistryBiochemistryISBN:9781319114671Author:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.Publisher:W. H. FreemanLehninger Principles of BiochemistryBiochemistryISBN:9781464126116Author:David L. Nelson, Michael M. CoxPublisher:W. H. FreemanFundamentals of Biochemistry: Life at the Molecul...BiochemistryISBN:9781118918401Author:Donald Voet, Judith G. Voet, Charlotte W. PrattPublisher:WILEY
- BiochemistryBiochemistryISBN:9781305961135Author:Mary K. Campbell, Shawn O. Farrell, Owen M. McDougalPublisher:Cengage LearningBiochemistryBiochemistryISBN:9781305577206Author:Reginald H. Garrett, Charles M. GrishamPublisher:Cengage LearningFundamentals of General, Organic, and Biological ...BiochemistryISBN:9780134015187Author:John E. McMurry, David S. Ballantine, Carl A. Hoeger, Virginia E. PetersonPublisher:PEARSON
Biochemistry
Biochemistry
ISBN:9781319114671
Author:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.
Publisher:W. H. Freeman
Lehninger Principles of Biochemistry
Biochemistry
ISBN:9781464126116
Author:David L. Nelson, Michael M. Cox
Publisher:W. H. Freeman
Fundamentals of Biochemistry: Life at the Molecul...
Biochemistry
ISBN:9781118918401
Author:Donald Voet, Judith G. Voet, Charlotte W. Pratt
Publisher:WILEY
Biochemistry
Biochemistry
ISBN:9781305961135
Author:Mary K. Campbell, Shawn O. Farrell, Owen M. McDougal
Publisher:Cengage Learning
Biochemistry
Biochemistry
ISBN:9781305577206
Author:Reginald H. Garrett, Charles M. Grisham
Publisher:Cengage Learning
Fundamentals of General, Organic, and Biological ...
Biochemistry
ISBN:9780134015187
Author:John E. McMurry, David S. Ballantine, Carl A. Hoeger, Virginia E. Peterson
Publisher:PEARSON