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Monoclonal antibodies are made by the fusion of cells of the immune system with B lymphocytes and myeloma cells.
<h3>What is Hybridoma technology?</h3>
- It is one of the best technologies that is used to produce the monoclonal antibody.
- In this hybridoma technology the B lymphocytes that are antibody producing are isolated from a source after the immunization with a specific antigen and then are fused with myeloma cell line to form hybrid cells that are also called as hybridoma cell lines.
- The hybridoma cell lines are then cultured in the laboratory with specific antigen and then the monoclonal antibodies are produced.
- This can be done in in-vivo or in-vitro condition.
- This method is preferred over all because the production of antibodies by this method is good as the antibodies produced are of high purity and highly sensitive and specific.
- These cell lines can also be preserved for a long time.
- Hybridoma technology has resulted in production of different varieties of monoclonal antibodies with specificity with specific antigens as the monoclonal antibodies are produced by single parental B cells.
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Long-term potentiation (LTP) is considered a cellular correlate of learning and memory. The presence of G protein-activated inwardly rectifying K(+) (GIRK) channels near excitatory synapses on dendritic spines suggests their possible involvement in synaptic plasticity. However, whether activity-dependent regulation of channels affects excitatory synaptic plasticity is unknown. In a companion article we have reported activity-dependent regulation of GIRK channel density in cultured hippocampal neurons that requires activity oF receptors (NMDAR) and protein phosphatase-1 (PP1) and takes place within 15 min. In this study, we performed whole-cell recordings of cultured hippocampal neurons and found that NMDAR activation increases basal GIRK current and GIRK channel activation mediated by adenosine A(1) receptors, but not GABA(B) receptors. Given the similar involvement of NMDARs, adenosine receptors, and PP1 in depotentiation of LTP caused by low-frequency stimulation that immediately follows LTP-inducing high-frequency stimulation, we wondered whether NMDAR-induced increase in GIRK channel surface density and current may contribute to the molecular mechanisms underlying this specific depotentiation. Remarkably, GIRK2 null mutation or GIRK channel blockade abolishes depotentiation of LTP, demonstrating that GIRK channels are critical for depotentiation, one form of excitatory synaptic plasticity.
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Answer:
Answer D
Explanation:
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Meiosis produce variations in daughter cells whereas mitosis produce identical nuclei.
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