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
The E3 ligase adaptor molecule SPOP regulates fetal hemoglobin levels in adult erythroid cells
Xianjiang Lan,Eugene Khandros,Peng Huang,Scott A. Peslak,Scott A. Peslak,Saurabh K. Bhardwaj,Jeremy D. Grevet,Jeremy D. Grevet,Osheiza Abdulmalik,Hongxin Wang,Cheryl A. Keller,Belinda Giardine,Josue Baeza,Emily R. Duffner,Osama El Demerdash,Xiaoli S. Wu,Xiaoli S. Wu,Christopher R. Vakoc,Benjamin A. Garcia,Ross C. Hardison,Junwei Shi,Gerd A. Blobel,Gerd A. Blobel +22 more
TL;DR: Speckle-type POZ protein (SPOP), a substrate adaptor of the CUL3 ubiquitin ligase complex, emerged as a novel HbF repressor and may offer new therapeutic strategies for the treatment of β-hemoglobinopathies.
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Rapid generation of drug-resistance alleles at endogenous loci using CRISPR-Cas9 indel mutagenesis
Jonathan J. Ipsaro,Chen Shen,Eri Arai,Yali Xu,Yali Xu,Justin B. Kinney,Leemor Joshua-Tor,Leemor Joshua-Tor,Christopher R. Vakoc,Junwei Shi +9 more
TL;DR: This method takes advantage of the heterogeneous in-frame alleles produced following Cas9-mediated DNA cleavage to generate rare alleles that confer resistance to the growth-arrest caused by chemical inhibitors and identifies novel resistance alleles of two lysine methyltransferases, DOT1L and EZH2, which are each essential for the growth of MLL-fusion leukemia cells.
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Miswired Enhancer Logic Drives a Cancer of the Muscle Lineage.
Berkley E. Gryder,Marco Wachtel,Kenneth Chang,Osama El Demerdash,Nicholas G. Aboreden,Wardah Mohammed,Winston Ewert,Silvia Pomella,Rossella Rota,Jun Wei,Young Min Song,Benjamin Z. Stanton,Beat W. Schäfer,Christopher R. Vakoc,Javed Khan +14 more
TL;DR: A hijacked enhancer network is revealed that disrupts the stepwise CR TF logic of normal skeletal muscle development (PAX3 to MYOD to MYOG), replacing it with an “infinite loop” enhancer logic that locks rhabdomyosarcoma in an undifferentiated stage.
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SMARCA2-deficiency confers sensitivity to targeted inhibition of SMARCA4 in esophageal squamous cell carcinoma cell lines.
Katharina Ehrenhöfer-Wölfer,Teresa Puchner,Cornelia Schwarz,Janine Rippka,Silvia Blaha-Ostermann,Ursula Strobl,Alexandra Hörmann,Gerd Bader,Stefan Kornigg,Stephan Karl Zahn,Wolfgang Sommergruber,Norbert Schweifer,Thomas Zichner,Andreas Schlattl,Ralph A. Neumüller,Junwei Shi,Christopher R. Vakoc,Manfred Kögl,Mark Petronczki,Norbert Kraut,Mark Pearson,Simon Wöhrle +21 more
TL;DR: The concept of SMARCA2/SMARCA4 paralog dependency is expanded and it is suggested that pharmacological inhibition of SMarCA4 represents a novel therapeutic opportunity for SMAR CA2-deficient cancers.
Journal ArticleDOI
Convergent organization of aberrant MYB complex controls oncogenic gene expression in acute myeloid leukemia
Sumiko Takao,Sumiko Takao,Lauren Forbes,Lauren Forbes,Lauren Forbes,Masahiro Uni,Masahiro Uni,Shuyuan Cheng,Shuyuan Cheng,Shuyuan Cheng,Jose Mario Bello Pineda,Yusuke Tarumoto,Yusuke Tarumoto,Paolo Cifani,Gerard Minuesa,Celine Chen,Michael G. Kharas,Michael G. Kharas,Robert K. Bradley,Christopher R. Vakoc,Richard Koche,Alex Kentsis,Alex Kentsis,Alex Kentsis +23 more
TL;DR: This paper showed that most subtypes of acute myeloid leukemia (AML) depend on the aberrant assembly of MYB transcriptional co-activator complex by rapid and selective peptidomimetic interference with the binding of CBP/P300 to myb, but not CREB or MLL1.