Work Description

Title: Data files for manuscript: "Regulation of STAT5-directed CD4+ T cell lineage commitment by the histone acetyltransferase Myst1" Open Access Deposited

http://creativecommons.org/licenses/by-nc/3.0/us/
Attribute Value
Methodology
  • Human samples, experimental animal models, mammalian cell culture, molecular biology
Description
  • Transcriptional accessibility of chromatin is central to guiding CD4+ T cell function through regulation of lineage specific gene expression. Myst1 is a histone acetyltransferase responsible for acetylation of the protein tail of histone 4 at lysine residue 16 (H416ac), resulting in increased transcriptional accessibility and activation of gene transcription. Previous studies have described a role for Myst1 in governing lymphocyte development in the thymus, however the role of Myst1 and H4K16ac in guiding activation of peripheral CD4+ T cells has not been studied. Activation of human and murine CD4+ T cells resulted in upregulation of Myst1 expression, and deletion of Myst1 resulted in changes in proliferative responses to both polyclonal stimulus and exogenous cytokines. Myst1-deficient T cells also exhibited modulations in lineage commitment, with decreased function in TH1/TH2 skewing conditions and increased function in response to TH17-promoting conditions. Regulation of Myst1 function in CD4+ T cells appears governed at least in part by STAT5, as Myst1 expression is regulated by STAT5 expression and DNA binding, and modulations in H4K16ac in Myst1-deficient CD4+ T cells is observable at sites in the promoter regions of lineage specific genes following skewing to the TH1 or TH2 lineage in vitro. Taken together, these results indicate an important role for the STAT5-Myst1 epigenetic axis in governing the activation and effector function of CD4+ T cells.
Creator
Depositor
  • wfcarson@umich.edu
Contact information
Discipline
Resource type
Last modified
  • 02/17/2020
Published
  • 08/04/2016
DOI
  • https://doi.org/10.7302/Z22F7KCH
License
To Cite this Work:
Carson, W. (2016). Data files for manuscript: "Regulation of STAT5-directed CD4+ T cell lineage commitment by the histone acetyltransferase Myst1" [Data set]. University of Michigan - Deep Blue. https://doi.org/10.7302/Z22F7KCH

Relationships

Files (Count: 198; Size: 440 MB)

Thumbnail Title Original Upload Last Modified File Size Access Actions
02.21.13 Human CD4 Donor 86&87 B...y.csv 2016-08-04 2016-08-04 9.84 KB Open Access
02.28.13 HuCD4 Skew Donor 88&89 ...d.csv 2016-08-04 2016-08-04 9.74 KB Open Access
1-17-12 DM CD4-Cre MOF CD4 Proli...2.pzf 2016-08-04 2016-08-04 190 KB Open Access
10-19-11 T cell skew Myst1.pzf 2016-08-04 2016-08-04 377 KB Open Access
10-19-11 T cell skew Myst1.xls 2016-08-04 2016-08-04 67.5 KB Open Access
10.19.11 TCell Skew (Pilot) Myst...).csv 2016-08-04 2016-08-04 1.85 KB Open Access
10.19.11 TCell Skew (Pilot) Myst...).csv 2016-08-04 2016-08-04 1.85 KB Open Access
10.19.11 TCell Skew (Pilot) Myst...).csv 2016-08-04 2016-08-04 1.31 KB Open Access
10.19.11 TCell Skew (Pilot) Myst...).csv 2016-08-04 2016-08-04 1.32 KB Open Access
10.19.11 TCell Skew (Pilot) Myst...).csv 2016-08-04 2016-08-04 1.32 KB Open Access
2-23-15 CD4-Cre Myst1 Skew resti...f.pzf 2016-08-04 2016-08-04 1.41 MB Open Access
2.12.13 Donor 84&85 Bradfor Assay.csv 2016-08-04 2016-08-04 9.4 KB Open Access
3-12-15 CD4-Cre Myst1 Skews & iT...n.pzf 2016-08-04 2016-08-04 1.23 MB Open Access
3-18-13 Cd4-Cre Myst1 BC KC Lys2...e.xls 2016-08-04 2016-08-04 152 KB Open Access
3-20-15 CD4-Cre Myst1 skew ChIP ...B.csv 2016-08-04 2016-08-04 2.97 KB Open Access
3-20-15 CD4-Cre Myst1 skew ChIP.pzf 2016-08-04 2016-08-04 693 KB Open Access
3-20-15 CD4-Cre Myst1 skew ChIP.xls 2016-08-04 2016-08-04 120 KB Open Access
3-20-15 CD4-Cre Myst1 T cell ske...A.csv 2016-08-04 2016-08-04 2.99 KB Open Access
3-23-15 CD4-Cre Myst1 skew ChIP ...5.csv 2016-08-04 2016-08-04 2.98 KB Open Access
3-24-15 CD4-Cre Myst1 skew ChIP ...4.csv 2016-08-04 2016-08-04 2.97 KB Open Access
3-24-15 CD4-Cre Myst1 skew ChIP ...5.csv 2016-08-04 2016-08-04 2.99 KB Open Access
3-6-14 CD4-Cre Myst1 ChIP GATA3 ...B.csv 2016-08-04 2016-08-04 3.03 KB Open Access
3-6-14 CD4-Cre Myst1 ChIP Tbx21 ...A.csv 2016-08-04 2016-08-04 2.99 KB Open Access
3-6-14 CD4-Cre Myst1 ChIP Tbx21 ...).csv 2016-08-04 2016-08-04 2.97 KB Open Access
3-6-14 CD4-Cre Myst1 ChIP.pzf 2016-08-04 2016-08-04 1.6 MB Open Access
3-6-14 CD4-Cre Myst1 ChIP.xls 2016-08-04 2016-08-04 112 KB Open Access
3-7-14 CD4-Cre Myst1 ChIP Foxp3 ...A.csv 2016-08-04 2016-08-04 2.96 KB Open Access
4-17-13 CD4-Cre Myst1 Flow .pzf 2016-08-04 2016-08-04 396 KB Open Access
4-17-13 CD4-Cre Myst1.jo 2016-08-04 2016-08-04 1.22 MB Open Access
9 16 15 beau sample 28-54 conc re.xml 2016-08-04 2016-08-04 44.8 KB Open Access
9 16 15 beau sample 28-54 conc.xml 2016-08-04 2016-08-04 20.4 KB Open Access
9-17-15 box 8 samp 28-54; rplp2,...).csv 2016-08-04 2016-08-04 1.61 KB Open Access
9-17-15 box 8 samp 28-54; rplp2,...).csv 2016-08-04 2016-08-04 1.58 KB Open Access
9-17-15 box 8 samp 28-54; rplp2,...).csv 2016-08-04 2016-08-04 1.58 KB Open Access
9-17-15 IL2 KO Restim.pzfx 2016-08-04 2016-08-04 288 KB Open Access
9-17-15 IL2 KO Restim.xls 2016-08-04 2016-08-04 52 KB Open Access
9.12.12 WT Stat5 Transfection Kn...).csv 2016-08-04 2016-08-04 9.43 KB Open Access
9.12.12 WT Stat5 Transfection Kn...).csv 2016-08-04 2016-08-04 1.74 KB Open Access
CD4-Cre Myst1 skews and restims.pzf 2016-08-04 2016-08-04 750 KB Open Access
Copy of Layout 1.tiff 2016-08-04 2016-08-04 20.2 MB Open Access
Donor 86&87 Analysis Western (40...).tif 2016-08-04 2016-08-04 12.9 MB Open Access
Donor 88&89.tif 2016-08-04 2016-08-04 14.1 MB Open Access
Donor 90 &93.tif 2016-08-04 2016-08-04 11.5 MB Open Access
Donor 90&93 HuCD4 Bradford.csv 2016-08-04 2016-08-04 9.68 KB Open Access
Human CD4 Skew Westerns Numerica....xlsx 2016-08-04 2016-08-04 51.9 KB Open Access
Human CD4 Western Numerical Anal....pzfx 2016-08-04 2016-08-04 32.9 KB Open Access
Image J analysis proof.tif 2016-08-04 2016-08-04 13.8 MB Open Access
Imager computer 2013-02-13 16hr ...c.scn 2016-08-04 2016-08-04 712 KB Open Access
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