L
Long Li
Researcher at California Institute of Technology
Publications - 7
Citations - 694
Long Li is an academic researcher from California Institute of Technology. The author has contributed to research in topics: Cellular differentiation & Gene regulatory network. The author has an hindex of 6, co-authored 7 publications receiving 625 citations.
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Journal ArticleDOI
An Early T Cell Lineage Commitment Checkpoint Dependent on the Transcription Factor Bcl11b
TL;DR: It is found that Bcl11b is necessary for T lineage commitment in mice and is specifically required both to repress natural killer cell–associated genes and to down-regulate a battery of stem cell or progenitor cell genes at the pivotal stage of commitment.
Journal ArticleDOI
A far downstream enhancer for murine Bcl11b controls its T-cell specific expression
Long Li,Jingli A. Zhang,Marei Dose,Hao Yuan Kueh,Ruzbeh Mosadeghi,Fotini Gounari,Ellen V. Rothenberg +6 more
TL;DR: Promoter-proximal and Major Peak sequences are cis-regulatory elements that interact over 850 kb to control expression of Bcl11b in hematopoietic cells.
Journal ArticleDOI
Multilayered specification of the T-cell lineage fate.
TL;DR: Insights into T‐cell specification and commitment that emerge from a combination of molecular, cellular, and systems biology approaches are reviewed and the regulatory structure underlying this lineage decision is revealed.
Journal ArticleDOI
Bcl11b and combinatorial resolution of cell fate in the T-cell gene regulatory network
William J.R. Longabaugh,Weihua Zeng,Jingli A. Zhang,Hiroyuki Hosokawa,Camden Jansen,Long Li,Maile Romero-Wolf,Pentao Liu,Hao Yuan Kueh,Ali Mortazavi,Ellen V. Rothenberg +10 more
TL;DR: It is shown that both activation and repression target genes can be bound by Bcl11b in vivo, and that B cl11b effects overlap with E2A-dependent effects, resolving how innate lymphoid, myeloid, and dendritic, and B-cell fate alternatives are excluded by different mechanisms.
Journal ArticleDOI
GATA-3 Dose-Dependent Checkpoints in Early T Cell Commitment
Deirdre D. Scripture-Adams,Sagar S. Damle,Long Li,Koorosh J. Elihu,Shuyang Qin,Alexandra M. Arias,Robert R. Butler,Ameya Champhekar,Jingli A. Zhang,Ellen V. Rothenberg +9 more
TL;DR: The pattern of GATA-3 expression sequentially produces B lineage exclusion, T lineage progression, and myeloid-lineage exclusion for commitment, as revealed by removing wild-type or Gata-3–deficient early T lineage cells from environmental Notch signals.