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IL-7R-dependent survival and differentiation of early T-lineage progenitors is regulated by the BTB/POZ domain transcription factor Miz-1.

Blood | Mar 24, 2011

http://www.ncbi.nlm.nih.gov/pubmed/21258009

T cells originate from early T lineage precursors that have entered the thymus and differentiate through well-defined steps. Mice deficient for the BTB/POZ domain of zinc finger protein-1 (Miz-1) almost entirely lack early T lineage precursors and have a CD4(-)CD8(-) to CD4(+)CD8(+) block causing a strong reduction in thymic cellularity. Miz-1(ΔPOZ) pro-T cells cannot differentiate in vitro and are unable to relay signals from the interleukin-7R (IL-7R). Both STAT5 phosphorylation and Bcl-2 up-regulation are perturbed. The high expression levels of SOCS1 found in Miz-1(ΔPOZ) cells probably cause these alterations. Moreover, Miz-1 can bind to the SOCS1 promoter, suggesting that Miz-1 deficiency causes a deregulation of SOCS1. Transgenic overexpression of Bcl-2 or inhibition of SOCS1 restored pro-T cell numbers and their ability to differentiate, supporting the hypothesis that Miz-1 is required for the regulation of the IL-7/IL-7R/STAT5/Bcl-2 signaling pathway by monitoring the expression levels of SOCS1.

Pubmed ID: 21258009 RIS Download

Mesh terms: Animals | Cell Differentiation | Cell Lineage | Cell Survival | Cells, Cultured | Gene Expression Regulation | Kruppel-Like Transcription Factors | Lymphoid Progenitor Cells | Mice | Mice, Inbred C57BL | Mice, Transgenic | Protein Structure, Tertiary | Receptors, Interleukin-7 | Suppressor of Cytokine Signaling Proteins | T-Lymphocytes | Transcription Factors | Zinc Fingers

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Associated grants

  • Agency: Canadian Institutes of Health Research, Id: 84526

Mouse Genome Informatics (Data, Gene Annotation)

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