Jenny Yan

Harvard University

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Scott Kennedy

Harvard University

Trever G. Bivona

UCSF Helen Diller Family Comprehensive Cancer Center

Elton Chan

UCSF Helen Diller Family Comprehensive Cancer Center

Victor Olivas

University of California, San Francisco

Luping Lin

Fujian Provincial Cancer Hospital

Saurabh Asthana

University of California, San Francisco

Evangelos Pazarentzos

UCSF Helen Diller Family Comprehensive Cancer Center

Marvin Wickens

University of Wisconsin–Madison

Amit J. Sabnis

University of California, San Francisco

Yuhan Fei

Center for Life Sciences

Cooperative Institutions

University of California, San Francisco

UCSF Helen Diller Family Comprehensive Cancer Center

Harvard University

University of Pennsylvania

Memorial Sloan Kettering Cancer Center

Johns Hopkins University

Massachusetts General Hospital

Howard Hughes Medical Institute

Sangamo BioSciences (United States)

City College of San Francisco

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poly(UG)-tailed RNAs in Genome Protection and Epigenetic Inheritance

bioRxiv (Cold Spring Harbor Laboratory) (2019)

Aditi Shukla Jenny Yan Daniel J. Pagano Anne E. Dodson Yuhan Fei

Abstract Mobile genetic elements threaten genome integrity in all organisms. MUT-2/RDE-3 is a ribonucleotidyltransferase required for transposon silencing and RNA interference (RNAi) in C. elegans . When tethered to RNAs in heterologous expression systems, RDE-3 can add long stretches of alternating non-templated uridine (U) and guanosine (G) ribonucleotides to the 3’ termini of these RNAs (polyUG or pUG tails). Here, we show that, in its natural context in C. elegans , RDE-3 adds pUG tails to transposon RNAs, as well as to targets of RNAi. pUG tails with more than 16 perfectly alternating 3’ U and G nucleotides convert otherwise inert RNA fragments into agents of gene silencing. pUG tails promote gene silencing by recruiting RNA-dependent RNA Polymerases (RdRPs), which use pUG-tailed RNAs as templates to synthesize small interfering RNAs (siRNAs). Cycles of pUG RNA-templated siRNA synthesis and siRNA-directed mRNA pUGylation underlie dsRNA-directed transgenerational epigenetic inheritance in the C. elegans germline. Our results show that pUG tails convert RNAs into transgenerational memories of past gene silencing events, which, we speculate, allow parents to inoculate progeny against the expression of unwanted or parasitic genetic elements.

RNA Silencing

Trans-acting siRNA

Piwi-interacting RNA

Small nucleolar RNA

RNA-induced silencing complex

10.1101/2019.12.31.891960

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Citations (4)

Long-term multilineage engraftment of autologous genome-edited hematopoietic stem cells in nonhuman primates

Blood (2016)

Christopher W. Peterson Jianbin Wang Krystin K. Norman Zachary K. Norgaard Olivier Humbert

Hematopoietic stem cell

10.1182/blood-2015-09-672337

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Citations (63)

The Hippo effector YAP promotes resistance to RAF- and MEK-targeted cancer therapies

Nature Genetics (2015)

Luping Lin Amit J. Sabnis Elton Chan Victor Olivas Lindsay Cade

Hippo signaling pathway

10.1038/ng.3218

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Citations (499)

β-GLUCAN ENHANCES HEMATOPOIETIC STEM CELL MOBILIZATION.

Journal of Investigative Medicine (2007)

Sabine Wagner Daniel Cramer R Hansen Ryan Reca Mariusz Z. Ratajczak

Mobilization

Hematopoietic stem cell

10.1097/00042871-200701010-00733

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Citations (0)

AXL Mediates Resistance to PI3Kα Inhibition by Activating the EGFR/PKC/mTOR Axis in Head and Neck and Esophageal Squamous Cell Carcinomas

Cancer Cell (2015)

Moshe Elkabets Evangelos Pazarentzos Dejan Juric Qing Sheng Raphael Pelossof

EGFR Inhibitors

10.1016/j.ccell.2015.03.010

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Citations (281)

NF-κB-Activating Complex Engaged in Response to EGFR Oncogene Inhibition Drives Tumor Cell Survival and Residual Disease in Lung Cancer

Cell Reports (2015)

Collin M. Blakely Evangelos Pazarentzos Victor Olivas Saurabh Asthana Jenny Yan

Although oncogene-targeted therapy often elicits profound initial tumor responses in patients, responses are generally incomplete because some tumor cells survive initial therapy as residual disease that enables eventual acquired resistance. The mechanisms underlying tumor cell adaptation and survival during initial therapy are incompletely understood. Here, through the study of EGFR mutant lung adenocarcinoma, we show that NF-κB signaling is rapidly engaged upon initial EGFR inhibitor treatment to promote tumor cell survival and residual disease. EGFR oncogene inhibition induced an EGFR-TRAF2-RIP1-IKK complex that stimulated an NF-κB-mediated transcriptional survival program. The direct NF-κB inhibitor PBS-1086 suppressed this adaptive survival program and increased the magnitude and duration of initial EGFR inhibitor response in multiple NSCLC models, including a patient-derived xenograft. These findings unveil NF-κB activation as a critical adaptive survival mechanism engaged by EGFR oncogene inhibition and provide rationale for EGFR and NF-κB co-inhibition to eliminate residual disease and enhance patient responses.

EGFR Inhibitors

Minimal Residual Disease

10.1016/j.celrep.2015.03.012

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Citations (180)

Co-Administration of Molecular Adjuvants Expressing NF-Kappa B Subunit p65/RelA or Type-1 Transactivator T-bet Enhance Antigen Specific DNA Vaccine-Induced Immunity

Vaccines (2014)

Devon J. Shedlock Colleen Tingey Lavanya Mahadevan Natalie A. Hutnick Emma L. Reuschel

DNA vaccine-induced immunity can be enhanced by the co-delivery of synthetic gene-encoding molecular adjuvants. Many of these adjuvants have included cytokines, chemokines or co-stimulatory molecules that have been demonstrated to enhance vaccine-induced immunity by increasing the magnitude or type of immune responses and/or protective efficacy. In this way, through the use of adjuvants, immune responses can be highly customizable and functionally tailored for optimal efficacy against pathogen specific (i.e., infectious agent) or non-pathogen (i.e., cancer) antigens. In the novel study presented here, we examined the use of cellular transcription factors as molecular adjuvants. Specifically the co-delivery of (a) RelA, a subunit of the NF-κB transcription complex or (b) T-bet, a Th1-specific T box transcription factor, along with a prototypical DNA vaccine expressing HIV-1 proteins was evaluated. As well, all of the vaccines and adjuvants were administered to mice using in vivo electroporation (EP), a technology demonstrated to dramatically increase plasmid DNA transfection and subsequent transgene expression with concomitant enhancement of vaccine induced immune responses. As such, this study demonstrated that co-delivery of either adjuvant resulted in enhanced T and B cell responses, specifically characterized by increased T cell numbers, IFN-γ production, as well as enhanced antibody responses. This study demonstrates the use of cellular transcription factors as adjuvants for enhancing DNA vaccine-induced immunity.

10.3390/vaccines2020196

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Citations (12)

The Kv1.3 potassium channel is localized to the cis‐Golgi and Kv1.6 is localized to the endoplasmic reticulum in rat astrocytes

FEBS Journal (2014)

Jing Zhu Jenny Yan William B. Thornhill

The functions of voltage-gated potassium (Kv) channels in neurons have been well defined, whereas their roles in glial cells are not fully understood. Kv1.1, Kv1.3 and Kv1.6 are endogenously expressed in C6 astrocytoma cells, but their trafficking and subcellular localization have not been well studied. In C6 cells, Kv1.1 was localized to the cell surface, Kv1.3 was predominantly localized in the cis-Golgi, and Kv1.6 was enriched in the endoplasmic reticulum. Disruption of the Golgi stacks with brefeldin A treatment redirected Kv1.3 to the endoplasmic reticulum, further confirming that Kv1.3 was localized in the Golgi. Denaturing and reducing immunoblot analysis identified an expected Kv1.3 monomer and an unexpected Kv1.3 dimer/aggregate. These two forms had different protein half-lives: that of the monomer form T1/2 was 5.1 h, whereas the dimer/aggregate form was stable over the 8-h measurement period. The Kv1.3 dimer/aggregate form on immunoblots appeared to be correlated with its Golgi retention, based on examination with several cell types that expressed Kv1.3. Glycosidase treatment showed that Kv1.3 contained complex-type N-glycans terminated with sialic acids, suggesting that Kv1.3 had traveled to the trans-Golgi network for sialylation before it was recycled to the cis-Golgi for retention. Inhibition of N-glycosylation did not affect Kv1.3 localization, indicating that N-glycans did not play a role in its Golgi retention. Thus, Kv1.3 appears to be distributed to the cis-Golgi membrane of rat astrocytes in a similar way as a Golgi resident protein, and this unusual distribution appears to be correlated with its SDS/2-mercaptoethanol-resistant dimer/aggregate forms on immunoblots.

Brefeldin A

10.1111/febs.12871

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Citations (39)

Clinical features and MRI characteristics of retinal detachment in dogs and cats

Veterinary Radiology & Ultrasound (2021)

Stephanie J. Stromberg Jenny Yan Tristan G. Wisner Erik R. Wisner Kathryn L. Good

Abstract The aim of this retrospective observational study was to characterize the MRI appearance of retinal detachment (RD) in a sample of dogs and cats. Study inclusion was based on the following medical record criteria: (a) had a diagnosis of RD in at least one eye by either funduscopic examination or ocular ultrasound and had an MRI evaluation including the eyes, or (b) had a diagnosis of RD documented in an MRI report for at least one eye and also had a clinical eye examination. Eighteen patients (12 dogs, 6 cats) and 35 eyes met the inclusion criteria, although four eyes that were clinically examined could not be visualized funduscopically and did not have ocular ultrasound performed (criterion 2). The MRI and clinical diagnosis (via either funduscopy or ultrasound) of RD/no RD was concordant in 27 of 31 eyes (87%). Qualitatively, RD appeared as a variable intensity curvilinear structure located internal and adjacent to the sclera on all sequences and was best delineated on T2W sequences. RDs inconsistently contrast enhanced and, although there was no statistical difference, subjectively appeared more clearly delineated on dorsal and parasagittal images. In conclusion, findings from the current study support using MRI as an ancillary diagnostic test for confirmation or further characterization of RD in dogs and cats.

Sclera

10.1111/vru.12999

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GABA receptor-channel complex as a target site of Mercury, copper, zinc, and lanthanides

Cellular and Molecular Neurobiology (1994)

Toshio Narahashi Jenny Yan Osamu Arakawa Eitan Reuveny Masanobu Nakahiro

Picrotoxin

Chloride channel

GABA receptor

10.1007/bf02088671

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Citations (59)