Monoclonal Anti-TIN2 (mouse IgG1 isotype) is derived from the hybridoma TIN-30 produced by the fusion of mouse myeloma cells and splenocytes from BALB/c mice immunized with a synthetic peptide corresponding to a fragment of human TIN-2, conjugated to keyhole limpet hemocyanin (KLH). The six shelterin subunits are: TRF1, TRF2, and POT1 which directly recognize the TTAGGG repeats, and TIN2, Rap1 and TPP1. TIN2 (TRF-1 interacting nuclear factor 2) is recruited to the telomere through the TRF homology (TRFH) domain of TRF1 and tethers TPP1/POT1 to TRF1 and TRF2.
애플리케이션
Monoclonal Anti-TIN2 antibody produced in mouse has been used in immunoblotting.
생화학적/생리학적 작용
TIN2 (TRF-1 interacting nuclear factor 2) also connects TRF1 to TRF2 and this link contributes to the stabilization of TRF2 on telomeres. In addition, TIN2 has also been found to tether the telomeres to the nuclear matrix. Interestingly, this protein has also been found to be mutated in Dyskeratosis Congenita, a multi-system disorder which in its classical form is characterized by abnormalities of the skin, nails, and mucous membranes.
물리적 형태
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
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Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Added by telomerase, arrays of TTAGGG repeats specify the ends of human chromosomes. A complex formed by six telomere-specific proteins associates with this sequence and protects chromosome ends. By analogy to other chromosomal protein complexes such as condensin and cohesin
The progressive bone marrow failure syndrome dyskeratosis congenita (DC) is often caused by mutations in telomerase or the factors involved in telomerase biogenesis and trafficking. However, a subset of DC patients is heterozygous for mutations in the shelterin component TIN2.
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