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DMS footprinting?|DMS footprinting method?|how DMS footprinting works?

                                                   DMS footprinting -         Dimethyl sulphate (DMS) is one of the oldest and most versatile chemical reagents used to probe RNA structure. -         It was introduced for RNA structure mapping in 1980. This early method allowed detection of methylation by DMS at N 7 of guanosine and N 3 of cytidine nucleotide because of modification facilitate cleavage of the chain. -         The sites of the methylation were determined by polyacrylamide gel electrophoresis (PAGE) analysis of end-labelled RNA. -         Analogous method was used to footprint the binding of protein to DNA. -         DMS footprinting is performed by binding the protein to its end labelled DNA target then attacking the DNA protein complex with DMS. -         DMS footprinting follows a similar principle as fingerprinting except that the DNA methylation agent DMS, instead of DNase. -         DMS foot printing which starts in the same ways as DNase foo

Detection of DNA binding ?

                                                Detection of DNA binding Radioisotope: - ·        Nucleic acid probe can be labelled using radioactive isotopes. ·        Most common process but less popular today become of safety consideration as well as coast and disposal of radio waste product. ·        However, radio labelled probes are the sensitive as they provide the highest degree of resolution currently available in hybridization assay. Non-radioactive labelled: - ·        Compared to radioactive labelled use of non-radioactive labelled have several advantages 1.     Safety. 2.     Highest stability of probe. 3.     Efficiency of labelling reaction. 4.     Detection incites. 5.     Less time taken to detect the signal. Some example as follows Biotin - this labelled can be detect using avidin or streptavidin which have high affinity for biotin. This type of non-radioactive labelled is known as an indirect system. Enzyme: - Enzyme is attach

Regulation of Immune response by|How is the immune system regulated?|

   Regulation of Immune response by – Antigen – 1.       T cell and B cell are triggered by antigen, after effective engagement of their antigen specific receptors together with appropriate constitution. 2.     In case of   T cell engagement is not with the antigen it self but with processed antigenic peptide bound to MHC I/II on APC. 3.     Effective immune response remove antigen from system repeated antigen exposure required to maintain T/B cell proliferation and during effective immune response, there is dramatic expansion of specifically reactive effector cell. 4.     Nature of antigen does and route of administration have influenced of development of immune response (IR) 5.     At the end of IR reduced antigen exposure result in reduced IL-2 expression and its receptor leading to apoptosis of antigen specific T cell. Following are some case under which tolerance is induced to foreign antigen. 1)     Nature/physical form of antigen: - The physical

Network theory and it`s experimental evidence|clona?l selection theory?

                Network theory and it`s experimental evidence -         Any discussion regarding of immune response not come to the end without mentioning Jern`s idiotype network theory. -         In 1973, Neil Jerne proposed this theory so to give possible solution for regulation of immune system in 1985 he was honored with Nobel prize for this work. -         This theory suggest that antigen enter the inside the body and activate very specific done of B cell secreting antibody against it. -         The antigen binding site of an antibody composed of overlap between light and heavy chain domain called as idiotype.         -         This recognizing are said to be complementary to antigen. -         Antibody molecule itself being a protein so can behave as an antigen. -         Antibody molecule against idiotype which exhibit internal image of an external antigen. -         Likewise, anti-ant idiotype antibody as external images of primary antibody. -