The ETS1 transcription factor is required for the development and cytokine-induced expansion of ILC2

Zook, Erin C.; Ramirez, Kevin; Guo, Xiaohuan; Voort, Grant van der; Sigvardsson, Mikael; Svensson, E. C.; Fu, Yang–Xin; Kee, Barbara L.

doi:10.1084/jem.20150851

Cited by 81 publications

(80 citation statements)

References 28 publications

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“…GATA‐3 expression is maintained at high levels in ILC2, unlike other ILC populations, and ILC2 remain dependent upon continued GATA‐3 expression for their function . ILC2 development is also dependent upon the transcription factors retinoic‐acid‐receptor‐related orphan receptor (ROR) α , Bcl11b and ETS‐1 …”

Section: Overview Of Ilc Groupsmentioning

confidence: 99%

Innate lymphoid cell regulation of adaptive immunity

Withers

2016

Immunology

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SummaryInnate lymphoid cells (ILCs) were identified principally as non-T-cell sources of key cytokines, able to provide rapid and early production of these molecules in the support of tissue homeostasis, repair and response to infection. As our understanding of these cells has developed, it has become evident that ILCs can impact on lymphocytes through a range of mechanisms. Hence, an exciting area of research has evolved in determining the extent to which ILCs may regulate adaptive immune responses. This review will focus initially on our current understanding of where ILC populations are located and what this means for potential cellular interactions. Mechanisms underpinning such interactions and how they may contribute to controlling adaptive immunity will then be considered.

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Section: Overview Of Ilc Groupsmentioning

confidence: 99%

Innate lymphoid cell regulation of adaptive immunity

Withers

2016

Immunology

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“…The rainbow color code describes the 3-D structures from the N-(blue) to C-termini (red color); predicted α-helices, β-sheets and proposed active site cleft are shown. activator BRG which controls transcription of genes important for the G1/S phase transition of the cell cycle [23]; STAT1, a signal transducer, transcription activator and modulator of retinoblastoma protein phosphorylation; RB1 (2 sites), retinoblastoma associated protein, and RBL2 (3 sites), are key regulators of entry into cell division [24]; ETS1, protein C-ets-1 transcription factor, which controls the expression of cytokine and chemokine genes [25]; and CTCF, CCCTC-binding factor, which organizes higher order chromatin structure, regulates gene expression and plays a role in learning and memory [26].…”

Section: Gene Locations Exonic Structures and Regulatory Sequences Fmentioning

confidence: 99%

Vertebrate Arylsulfatase K (ARSK): Comparative and Evolutionary Studies of the Lysosomal 2-Sulfoglucuronate Sulfatase

Holmes¹

2018

J Data Mining Genomics Proteomics

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Arylsulfatase K (ARSK) is one of 17 sulfatase gene family members encoded on the human genome for which a role has been recently identified as a lysosomal 2-sulfoglucuronate sulfatase. Vertebrate ARSK sequences shared 60-82% identity but only <27% identities with other arylsulfatase family members. Comparative enzyme structures were studied, including residues with predicted roles in forming N-glycosylation sites, Ca 2+ binding and active site residues. Vertebrate ARSK genes usually contained 8 coding exons. A human ARSK gene promoter comprised CpG61 and multiple TFBS, which may be involved in signal transduction, transcription activation or regulating entry into cell division. Phylogenetic analyses examined evolutionary changes for the vertebrate ARSK and the invertebrate SUL1 genes. In summary, a major role for this enzyme as a 2-sulfoglucuronate sulfatase is supported which has been conserved throughout vertebrate evolution.Citation: Holmes RS (2017) Vertebrate Arylsulfatase K (ARSK): Comparative and Evolutionary Studies of the Lysosomal 2-Sulfoglucuronate Sulfatase.

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“…11,12 CHILP depend upon the transcription factor ETS1 for appropriate fitness. 13 Expression of PLZF (promyelocytic leukemia zinc finger) protein and the upregulation of the cell surface receptor PD-1 (programmed death 1) marks the differentiation of CHILP into ILCP, which can repopulate all helper ILC lineages but not LTi cells. 14,15 ILC development requires IL-2, IL-7, and Notch signaling 5,6,16–19 , whereas RAG (recombination-activating gene) expression is dispensable consistent with a lack of antigen specificity in ILC.…”

Section: Ilc Developmentmentioning

confidence: 99%