scispace - formally typeset
L

Lee Rowen

Researcher at Institute for Systems Biology

Publications -  65
Citations -  35324

Lee Rowen is an academic researcher from Institute for Systems Biology. The author has contributed to research in topics: Gene & Genome. The author has an hindex of 39, co-authored 62 publications receiving 32743 citations. Previous affiliations of Lee Rowen include University of Washington & California Institute of Technology.

Papers
More filters
Journal ArticleDOI

Molecular dissection of prethymic progenitor entry into the T lymphocyte developmental pathway.

TL;DR: A major fraction of these early T lineage genes are a regulatory legacy from stem cells, including zinc finger transcription factor, helicase, and signaling adaptor genes, which was also shared by stem cells and multipotent progenitors, although down-regulated in other lineages.
Journal ArticleDOI

Transcription factor expression dynamics of early T-lymphocyte specification and commitment

TL;DR: T-cell identity has an essentially complex regulatory basis and a detailed framework for regulatory network modeling of T-cell specification is provided.
Journal ArticleDOI

Cloning, Characterization, and the Complete 56.8-Kilobase DNA Sequence of the Human NOTCH4 Gene

TL;DR: The first complete mammalian genomic sequence reported thus far in the Notch gene family, including a putative promoter region and 30 exons of the human NOTCH4 gene spanning 56.8 kb of DNA, were sequenced.
Journal ArticleDOI

The risk of COVID-19 death is much greater and age dependent with type I IFN autoantibodies

Jeremy Manry, +178 more
TL;DR: It is found that autoantibodies against type I IFNs strongly increased the SARS-CoV-2 infection fatality rate at all ages, in both men and women.
Journal ArticleDOI

Analysis of the DNA sequence and duplication history of human chromosome 15

TL;DR: A detailed analysis of the duplication structure of human chromosome 15 finds that most of the intrachromosomal duplications seem to share a common ancestry, and demonstrates that some remaining gaps in the genome sequence are probably due to structural polymorphisms between haplotypes.