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Intron-mediated enhancement (IME) is the ability of an intron sequence to enhance the expression of a gene containing that intron. In particular, the intron must be present in the transcribed region of the gene for enhancement to occur, differentiating IME from the action of typical transcriptional enhancers . [ 1 ]
Immunotherapy or biological therapy is the treatment of disease by activating or suppressing the immune system. Immunotherapies designed to elicit or amplify an immune response are classified as activation immunotherapies, while immunotherapies that reduce or suppress are classified as suppression immunotherapies .
[7] [8] [9] This enhancer, located in the large intron, provided an explanation for the transcriptional activation of rearranged Vh gene promoters while unrearranged Vh promoters remained inactive. [10] Lately, enhancers have been shown to be involved in certain medical conditions, for example, myelosuppression. [11]
There are two main categories of immunostimulants: [1] Specific immunostimulants provide antigenic specificity in immune response, such as vaccines or any antigen.; Non-specific immunostimulants act irrespective of antigenic specificity to augment immune response of other antigen or stimulate components of the immune system without antigenic specificity, such as adjuvants and non-specific ...
An intron is any nucleotide sequence within a gene that is not expressed or operative in the final RNA product. The word intron is derived from the term intragenic region, i.e., a region inside a gene. [1] The term intron refers to both the DNA sequence within a gene and the corresponding RNA sequence in RNA transcripts. [2]
This makes gene trapping more easily amenable for large scale projects than targeting. On the other hand, gene targeting can be used for genes with low transcriptions that would go undetected in a trap screen. The probability of trapping increases with intron size, while for gene targeting, small genes are just as easily altered.
During RNA splicing, U2 small nuclear RNA auxiliary factor 1 (U2AF35) and U2AF2 (U2AF65) interact with the branch site and the 3' splice site of the intron to form the lariat. It is thought that SR proteins that bind to ESEs promote exon splicing by increasing interactions with U2AF35 and U2AF65.
Autologous immune enhancement therapy; Autophagy; B. Beta-2 microglobulin; Binding antibody; ... Interferon beta 1a; Interferon beta 1b; Interferon gamma; Interferon ...