Charles Y. Lin

Baylor College of Medicine

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Albert Chin

National Yang Ming Chiao Tung University

James E. Bradner

Dana-Farber Cancer Institute

Peter B. Rahl

Fulcrum Therapeutics (United States)

Behnam Nabet

Fred Hutch Cancer Center

Tamara D. Hopkins

Boehringer Ingelheim (United States)

David A. Orlando

Orlando Science Center

Nikolaus D. Obholzer

Harvard University

B. Wesley Trotter

PathAI (United States)

S. P. McAlister

CytomX Therapeutics (United States)

Christopher J. Dinsmore

Forma Therapeutics (United States)

Cooperative Institutions

Harvard University

Dana-Farber Cancer Institute

Massachusetts Institute of Technology

Baylor College of Medicine

Broad Institute

Boston Children's Hospital

Brigham and Women's Hospital

Whitehead Institute for Biomedical Research

Texas Children's Hospital

Dana-Farber/Boston Children's Cancer and Blood Disorders Center

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Abstract 198: DNA Base Editing in Hutchinson-Gilford Progeria Syndrome

Arteriosclerosis Thrombosis and Vascular Biology (2019)

Luke W. Koblan Sean Doherty Jon M Levy Michael R. Erdos Francis S. Collins

Background: Children afflicted with Hutchinson-Gilford Progeria Syndrome (HGPS) die from progressive vascular disease at an average age of 14. Despite elucidation of the genetic cause—C1824T point ...

Progeria

Base (topology)

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Feature modification framework for feature based design systems

International Journal of Production Research (1995)

Rong-Kwei Li Charles Y. Lin Huiyan Wu

Abstract Design features created by a feature based design system could theoretically be directly sent to machining preparation system. This, however, has not been found and feature modification is still necessary. A feature modification framework is proposed in this paper for bridging the gap between the design features and machining features. Feature modification algorithms were also developed for the foundation of the framework. A prototype system is presented and illustrated by an explanation of how the feature modification concept could function in a real situation.

Feature (linguistics)

Feature model

Feature recognition

10.1080/00207549508930165

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Citations (9)

Strong and efficient light emission in ITO/Al/sub 2/O/sub 3/ superlattice tunnel diode

Albert Chin Chun-Jie Liang Charles Y. Lin Chu-Chun Wu J. Liu

We have studied the electroluminescence of ITO/Al/sub 2/O/sub 3/ superlattice tunnel diode on Si. The light emission intensity and efficiency are >3 orders of magnitude larger than 20 /spl Aring/ SiO/sub 2/ tunnel diode and 0.18 /spl mu/m MOSFET. Besides the small 3 V operation and low power consumption, good reliability is another merit for this device.

Figure of Merit

10.1109/iedm.2001.979459

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Citations (1)

Strong and efficient light emission in ITO/Al2O3 superlattice tunnel diode

International Electron Devices Meeting (2001)

Albert Chin Chenhui Liang Charles Y. Lin C. C. Wu J. Liu

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Citations (6)

Multi-Omic Transcription Regulatory Network Mapping Identifies Targetable Oncogenic TF-Cofactor Relationship between IRF4 and p300 in Multiple Myeloma, and Is Used to Improve TF Protein-Protein Interaction Methodology

Blood (2024)

Yupeng Zheng Walter F. Lenoir M.J. Kobylarz Jun Li Tamara D. Hopkins

IRF4

MYB

Chromatin immunoprecipitation

10.1182/blood-2024-210684

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Abstract 131: A microRNA Targets the Epigenetic Reader BRD4 to Suppress Transcription Elongation in the Heart

Circulation Research (2015)

Matthew S. Stratton Bradley S. Ferguson Charles Y. Lin Priti Anand Sean T. Wickers

BRD4 is a member of the BET family of proteins, which contain tandem reader domains (bromodomains) that bind to acetylated histone tails within chromatin. We recently demonstrated that JQ1, a small molecule that prevents BRD4-chromatin interaction, potently blocks pathological cardiac hypertrophy and improves cardiac function in pre-clinical models. BRD4 functions as a nodal regulator of the transcriptional program for cardiac hypertrophy by recruiting P-TEFb to gene regulatory elements, resulting in phosphorylation of RNA polymerase II (Pol II), and subsequent transcription elongation. Here, we describe a signal-dependent mechanism for regulation of BRD4 in the heart. BRD4 protein expression is dramatically upregulated in cardiomyocytes exposed to cues for pathological, but not physiological, hypertrophy. In unstimulated cardiomyocytes, BRD4 protein expression is maintained at low levels by a microRNA, which directly targets the 3’ UTR of the BRD4 transcript, thereby preventing translation of this acetyl-lysine reader. In response to signals for hypertrophy, expression of the microRNA is down regulated through a histone deacetylase (HDAC)-dependent mechanism, resulting in robust induction of BRD4 protein synthesis. Whole genome analyses establish a crucial role for the microRNA in the control of Pol II elongation in the heart via BRD4 down regulation. These findings define a novel chromatin signaling axis that can be targeted at multiple levels (epigenetic reader, microRNA or HDAC) for the treatment of heart failure.

BRD4

RNA polymerase II

10.1161/res.117.suppl_1.131

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Light Emission Near 1.3 m Using ITO-Al O -Si Ge -Si Tunnel Diodes

Charles Y. Lin Albert Chin Yunfei Hou M. F. Li S. P. McAlister

We have fabricated Sn : In O (ITO)-Al O dielec- tric on Si Ge -Si metal-oxide-semiconductor tunnel diodes which emit light at around 1.3 m, for . The emitted photon energy is smaller than the bandgap energy of Si, thus, avoiding strong light absorption by the Si substrate. The optical device structure is compatible with that of a metal-oxide-semicon- ductor field-effect transistor, since a conventional doped poly-Si gate electrode will be transparent to the emitted light. Increasing the Ge composition from 0.3 to 0.4 only slightly decreases the light-emitting efficiency.

Light emission

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PI3K/AKT Signaling Regulates H3K4 Methylation in Breast Cancer

Cell Reports (2016)

Jennifer M. Spangle Koen M.A. Dreijerink Anna C. Groner Hailing Cheng Carolynn E. Ohlson

Post-translational histone H3 modifications regulate transcriptional competence. The mechanisms by which the epigenome is regulated in response to oncogenic signaling remain unclear. Here we show that H3K4me3 is increased in breast tumors driven by an activated PIK3CA allele and that inhibition of PI3K/AKT signaling reduces promoter-associated H3K4me3 in human breast cancer cells. We show that the H3K4 demethylase KDM5A is an AKT target and that phosphorylation of KDM5A regulates its nuclear localization and promoter occupancy. Supporting a role for KDM5A in mediating PI3K/AKT transcriptional effects, the decreased expression in response to AKT inhibition of a subset of cell-cycle genes associated with poor clinical outcome is blunted by KDM5A silencing. Our data identify a mechanism by which PI3K/AKT signaling modulates the cancer epigenome through controlling H3K4 methylation and suggest that KDM5A subcellular localization and genome occupancy may be pharmacodynamic markers of the activity of PI3K/AKT inhibitors currently in clinical development.

10.1016/j.celrep.2016.05.046

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Citations (105)

Light emission in (La, Al)/sub 2/O/sub 3//Si MOS tunnel diodes

Charles Y. Lin H.Y. Lee Albert Chin

Efficient light emission from (La, Al)/sub 2//Si MOS tunnel diodes with photon energies ranging from 1.4 to 1.6 eV was demonstrated. This novel technology should find wide applications in optical interconnects and wireless communications.

Ranging

Light emission

10.1109/cleopr.2003.1277163

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Signal-Dependent Recruitment of BRD4 to Cardiomyocyte Super-Enhancers Is Suppressed by a MicroRNA

Cell Reports (2016)

Matthew S. Stratton Charles Y. Lin Priti Anand Philip D. Tatman Bradley S. Ferguson

BRD4 governs pathological cardiac gene expression by binding acetylated chromatin, resulting in enhanced RNA polymerase II (Pol II) phosphorylation and transcription elongation. Here, we describe a signal-dependent mechanism for the regulation of BRD4 in cardiomyocytes. BRD4 expression is suppressed by microRNA-9 (miR-9), which targets the 3′ UTR of the Brd4 transcript. In response to stress stimuli, miR-9 is downregulated, leading to derepression of BRD4 and enrichment of BRD4 at long-range super-enhancers (SEs) associated with pathological cardiac genes. A miR-9 mimic represses stimulus-dependent targeting of BRD4 to SEs and blunts Pol II phosphorylation at proximal transcription start sites, without affecting BRD4 binding to SEs that control constitutively expressed cardiac genes. These findings suggest that dynamic enrichment of BRD4 at SEs genome-wide serves a crucial role in the control of stress-induced cardiac gene expression and define a miR-dependent signaling mechanism for the regulation of chromatin state and Pol II phosphorylation.

BRD4

RNA polymerase II

Transcription

10.1016/j.celrep.2016.06.074

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Citations (72)