C
Christopher R. Vakoc
Researcher at Cold Spring Harbor Laboratory
Publications - 153
Citations - 21315
Christopher R. Vakoc is an academic researcher from Cold Spring Harbor Laboratory. The author has contributed to research in topics: Transcription factor & Chromatin. The author has an hindex of 52, co-authored 132 publications receiving 17071 citations. Previous affiliations of Christopher R. Vakoc include University of Pennsylvania & Watson School of Biological Sciences.
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Journal ArticleDOI
Made to order tuft cells by an OCA-T1 isoform switch
TL;DR: In this article , a genetic mechanism accounts for the variation in tuft cell abundance seen among inbred mouse strains: alternative isoforms of OCA-T1 (Oct coactivator from tuft cells 1), a recently discovered transcriptional co-activator that specifies the tuftcell lineage.
Journal ArticleDOI
Abstract IA011: Transcriptional dependencies of tuft cell lung tumors
TL;DR: Vakoc et al. as mentioned in this paper used genetic screens performed in cancer cell lines to identify a tuft cell variant of small cell lung cancer, which is characterized by high expression of, and addiction to, POU2F3.
Posted ContentDOI
p73 activates transcriptional signatures of basal lineage identity and ciliogenesis in pancreatic ductal adenocarcinoma
Stella K Hur,Tim D.D. Somerville,Xiaoli S. Wu,Diogo Maia-Silva,Osama El Demerdash,David A. Tuveson,Faiyaz Notta,Christopher R. Vakoc +7 more
TL;DR: In this article , a subset of pancreatic ductal adenocarcinoma (PDAC) tumors aberrantly express p73 (TA isoform), which is a known transcriptional activator of basal lineage identity, ciliogenesis, and tumor suppression in normal tissue development.
Posted ContentDOI
The SCP4-STK35/PDIK1L complex is a dual phospho-catalytic signaling dependency in acute myeloid leukemia
Sofya A. Polyanskaya,Moreno Ry,Bin Lu,Ruopeng Feng,Yu Yao,Seema Irani,Olaf Klingbeil,Zhaolin Yang,Yiliang Wei,Osama El Demerdash,Benjamin La,Mitch Weiss,Yan Zhang,Christopher R. Vakoc +13 more
TL;DR: A phosphatase-kinase signaling complex that supports the pathogenesis of AML is revealed, with evidence that SCP4 regulates STK35/PDIK1L through two distinct mechanisms: catalytic removal of inhibitory phosphorylation and by promoting kinase stability.
Journal ArticleDOI
In vivo CRISPR/Cas9 Screening Identifies Pbrm1 as a Regulator of Mouse Myeloid Leukemia Development.
TL;DR: In this paper , a pooled CRISPR/Cas9 editing of genes encoding epigenetic factors and identified Pbrm1/Baf180, a subunit of polybromo BRG1/BRM-associated factor (PBAF) SWI/SNF chromatin remodeling complex, as negative driver of disease progression.