癌症科学与研究杂志

癌症科学与研究杂志
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国际标准期刊号: 2576-1447

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TAL和LYL1转录因子相关肿瘤发生的生物信息学分析

舒哈萨·乔杜里

The present study investigated the common primary tumors-specific alteration of the TALI gene induces almost 25% of patients with T-cell acute lymphoblastic leukemia. The TAL gene product induces a helix-loop-helix transcription factor especially homologous to the LYL1. TAL1, TAL2, and LYL1 constitute discrete subgroup bHLH transcription factor potential contribution to the development of T-cell oncogenesis. The TAL2 translocated chromosome 9 breakpoint of t (7; 9) (q34; 7. q32) especially associated with T-cell. The TAL2 is juxtaposed with sequences from the T-cell receptor beta-chain gene on a chromosome 7. The sequence homologs TAL1, TAL2, and LYL1 are conserved during evolution. The TAL1, TAL2, and LYL1 constitute a unique family of bHLH transcription factor potential mediator of T-cell leukaemogenesis. TAL1, TAL2, and LYL1 encode a helix-loop-helix transcription factor involved in the malignant development of lymphocytes. We accumulate eukaryotes organism i.e. Homo sapiens and Mus musculus for comparative and functional analysis. Our data provide evidence that the total 6, 2, 2 TAL1, TAL2, and LYL1 in Homo sapiens and Mus musculus respectively including domain, motifs, phylogeny, chromosome location, and gene expression. In this study, we performed bioinformatics and computational analysis to validate the current knowledge of the TAL1, TAL2 and LYL1 transcription factor

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