Elucidating altered transcriptional programs multiple choice questions for dating

Natural killer T (NKT) cells are a specialized population of innate-like T cells that acquire their effector program during development under the control of the transcription factor PLZF (promyelocytic leukemia zinc finger, encoded by ).

To elucidate the mechanisms underlying this unique property of PLZF, we performed Ch IP-seq and microarray analysis of NKT cells and PLZF-transgenic T cells, which revealed direct regulation of effector genes and of T-helper–specific transcription factors.

However, the mechanistic aspects of SMYD3 transactivation and whether SMYD3 acts in concert with other transcription modulators remain unclear.

Here, we show that SMYD3 interacts with the human positive coactivator 4 (PC4) and that such interaction potentiates a group of genes whose expression is linked to cell proliferation and invasion.

Whereas C57BL/6 mice produce predominantly NKT cells with a T-bet–dependent type 1 helper phenotype (NKT1), other strains, including BALB/c, also express substantial populations of so-called NKT2 and NKT17 cells with polarized type 2 and type 17 helper programs controlled by GATA3 and RORγt, respectively.

The BTB-zinc finger transcription factor PLZF (promyelocytic leukemia zinc finger, encoded by ), is specifically expressed in NKT cells, but not in conventional T cells or NK cells, and directs the acquisition of several key components of the NKT cell effector program during development, including cytokine and migration properties (4 abrogate both the expansion and the effector-memory differentiation of NKT cells, resulting in reversal to a naive phenotype and redistribution to the lymph nodes and circulating blood.

Using biotinylation-based Ch IP-seq and microarray analysis of both natural killer T (NKT) cells and PLZF-transgenic thymocytes, we identified several layers of regulation of the innate-like NKT effector program.

The most frequent genetic abnormality in T-ALL is the dysregulation of transcription factor genes.

We previously identified the “core transcriptional regulatory circuits” controlled by the oncogenic transcription factor TAL1 in T-ALL.

My long-term goal is to improve cancer cure rates by developing novel therapeutics.

To meet this challenge, I have been studying T-cell acute lymphoblastic leukemia (T-ALL) and other lymphoid malignancies.

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