What is the difference, at the molecular level, among the A, B, and O antigens? A - N-acetylgalactosamine is terminal sugar B - Galactose is terminal sugar O - No terminal sugar

The ends of each heavy chain and light chain in an immunoglobulin make up the antigen-binding sites. The end of one of these chains is shown here.     Biochemists tend to classify protein structures into four groups: mostly alpha, mostly beta, mixed alpha and beta, or neither alpha nor beta. Based on the model shown here, how would you classify this part of the immunoglobulin protein? The loopy polypeptide segments at the very top of the structure shown are the segments that actually contact the antigen. Would you expect these binding segments to be rigid or flexible?

================================(Wearing a face mask, hand hygiene, and social distance); all of these are ways to break the chain of COVID-19. a.False. b.True. ================================Mosquitoes: are often carriers of biological vector-borne transmission; multiplication and development of the organism may not occurs. a.True. b.False.

how can we protect others and ourselves if we don't know who is infected with covid-19?

Antibody heavy and light chain polypeptides consist of repeated domains, each of which is ~110 amino acids and folds up into a compact three-dimensional structure known as an ‘immunoglobulin domain.’ These immunoglobulin domains are: Mixed and matched between different antibody heavy and light chains to produce variability Always identical to each other within a single antibody heavy chain or light chain polypeptide Always differ in amino acid sequence between different light chain polypeptides in both of the two light chain immunoglobulin domains Similar but not identical in amino acid sequence when comparing the domains in a single heavy chain polypeptide Identical in amino acid sequence for every domain when comparing different antibody heavy chain polypeptides to each other

Which antibody type description among A- D is falsely characterized? A) O IgA: form dimers; prevent adherence of pathogens to mucosal surfaces 1f1 B) O IgG: circulating antibody with multiple functions; formed in high numbers in secondary antibody response C) O IgM: forms multimers whose function is agglutination of infectious microbes D) O IgE, IgD: carry out their function while bound to the surfaces of specific cell types E) O None are false, A-D are all correct

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 drug

The mechanism of cross-presentation by dendritic cells is an essential pathway for generating CD8 T cell responses to some intracellular pathogens. If this pathway did not exist, we would be highly susceptible to: Intracellular pathogens that can survive inside macrophage endocytic vesicles Intracellular pathogens that are able to evade antibody responses Intracellular pathogens that do not infect and replicate in dendritic cells Intracellular pathogens that can spread from cell to cell by inducing cell fusion Intracellular pathogens that infect and replicate in red blood cells

1.27 Results of complementation tests of the six indepen- dent recessive mutations a-f are shown in the accompanying matrix, where + indicates comple- mentation and – indicates lack of complementa- tion. Classify the mutations into complementation groups, and write the names of the mutations in luen

The formation of the C3 convertase is a key step in complement activation that occurs in all three complement pathways. This enzyme cleaves C3 in blood plasma, leading to a conformational change in the C3b fragment that exposes its reactive thioester group. The activated C3b is potentially harmful to the host, if it becomes covalently attached to a host cell, rather than to the surface of a pathogen. This deleterious outcome is largely avoided by:  The inability of active C3b to diffuse away in the blood plasma. The inability of active C3b to covalently attach to the membranes of eukaryotic cells. The rapid hydrolysis of active C3b in solution, rendering it inactive. The tight binding of active C3b to the C3 convertase. The ability of active C3b to recruit phagocytic cells.