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Computational Analysis of Single Nucleotide polymorphisms (SNPs) in Human T-Cell Acute Lymphocytic Leukemia Protein 1 (TAL1) Gene/ Comprehensive Study

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Background: TAL1 is a proto-oncogene whose distorted modifications in committed T-cell Precursors is related with the development of T-ALL, it also found to be related to many other human hematological diseases such as lymphoblastic lymphoma, immunodeficiency 18, acute myeloid leukemia and diamond-blackfan Anemia. Objectives: This study aims to predict the effect of nsSNPs on TAL1 protein structure function  Methods: Retrieved nSNPs in the coding and 3’UTR regions were analyzed using different in silico tools. Interactions of TAL1 with functionally similar genes were investigated using Genemania. Post-translational modifications in several sites of the protein were also investigated.  Results: Out of ninety nsSNPs identified, only eight were found damaging to protein function of which one is located in the basis helix-loop-helix domain (bHLH). Two SNPs were anticipated by PolymiRTs to prompt disturbance or creation of miR binding sites. Conclusion: The present study is the first ever computational analysis of TAL1’s nsSNPs hence this effort might be of help in the near future for inventing early diagnostic and therapeutic measures for T-ALL
Title: Computational Analysis of Single Nucleotide polymorphisms (SNPs) in Human T-Cell Acute Lymphocytic Leukemia Protein 1 (TAL1) Gene/ Comprehensive Study
Description:
Background: TAL1 is a proto-oncogene whose distorted modifications in committed T-cell Precursors is related with the development of T-ALL, it also found to be related to many other human hematological diseases such as lymphoblastic lymphoma, immunodeficiency 18, acute myeloid leukemia and diamond-blackfan Anemia.
Objectives: This study aims to predict the effect of nsSNPs on TAL1 protein structure function  Methods: Retrieved nSNPs in the coding and 3’UTR regions were analyzed using different in silico tools.
Interactions of TAL1 with functionally similar genes were investigated using Genemania.
Post-translational modifications in several sites of the protein were also investigated.
  Results: Out of ninety nsSNPs identified, only eight were found damaging to protein function of which one is located in the basis helix-loop-helix domain (bHLH).
Two SNPs were anticipated by PolymiRTs to prompt disturbance or creation of miR binding sites.
Conclusion: The present study is the first ever computational analysis of TAL1’s nsSNPs hence this effort might be of help in the near future for inventing early diagnostic and therapeutic measures for T-ALL.

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