Zhang 2022

Ying E. Zhang, Ph.D.

  • Center for Cancer Research
  • National Cancer Institute


Dr. Zhang's research focuses on understanding TGF-beta signaling and functions of ubiquitin E3 ligase Smurfs. She identified and characterized several key molecules in the TGF-beta signaling pathway, including Smads and Smurfs. Discoveries from her group generated mechanistic insight into how TGF-beta controls cellular responses through Smad-dependent and -independent pathways in normal and cancer cells. On the front of Smurf E3 ligases, their findings extended the function of Smurfs beyond TGF-beta pathway to genome stability and metastasis.

Areas of Expertise

TGF-Beta Signaling
Protein Kinases
Mouse Models


Selected Key Publications

TGF-β-induced Alternative Splicing of TAK1 Promotes EMT and Drug Resistance

Tripathi V, Shin JH, Stuelten CH, Zhang YE.
Oncogene. 38(17): 3185-3200, 2019. [ Journal Article ]

Mechanistic Insight Into Contextual TGF-β Signaling

Zhang YE.
Curr Opin Cell Biol. 51: 1-7, 2018. [ Journal Article ]

Non-proteolytic ubiquitin modification of PPARγ by Smurf1 protects the liver from steatosis

Zhu K, Tang Y , Xu X , Dang H , Tang LY , Wang X, Wang XW , Zhang YE
PLOS Biology. 16(12): e3000091, 2018. [ Journal Article ]

Transforming Growth Factor-β (TGF-β) Directly Activates the JAK1-STAT3 Axis to Induce Hepatic Fibrosis in Coordination with the SMAD Pathway

Tang LY, Heller M, Meng Z, Yu LR, Tang Y, Zhou M, Zhang YE.
J Biol Chem. 292(10): 4302-12, 2017. [ Journal Article ]

Direct Regulation of Alternative Splicing by SMAD3 through PCBP1 Is Essential to the Tumor-Promoting Role of TGF-beta.

Tripathi V, Sixt KM, Gao S, Xu X, Huang J, Weigert R, Zhou M, Zhang YE.
Molecular Cell. 64(5): 1010, 2016. [ Journal Article ]

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Xiao from 2022 Group photo
Staff Scientist
TiaoJiang Xiao, Ph.D.
Yi ppt from group wall
Yi Tang, Ph.D.
Jeehye pic from group wall
Research Fellow (Visiting)
Jee-Hye Shin, Ph.D.
Birendra photo from group wall
Postdoctoral Fellow (CRTA)
Birendra Kc, Ph.D.
Postdoctoral Fellow (Visiting)
Md Rasel Molla, Ph.D.
Hannah from group photo wall
Postbaccalaureate Fellow (CRTA)
Hannah Kim, B.S.


Ying Zhang’s research featured in NIH Intramural Research Program blog The blog post, “Scientific Detour Advances Understanding of Fatty Liver Disease," focuses on Dr. Zhang’s research, including a recent study that could eventually lead to preventing or reversing unhealthy amounts of fat storage in the liver.   Read more...

Ying Zhang was elected to the 2021 class of American Association for the Advancement of Science (AAAS) Fellows.


Cancer-Fighting Smurf on the Chromatin

A tumor suppressor function of Smurf2 associated with controlling chromatin landscape and genome stability through RNF20

Published Date

About the Cover:

The cover shows the co-localization of Smurf2 with DNA damage markers in the nuclei of human osteosarcoma cells.


In addition to allelic mutations, cancers are known to harbor alterations in their chromatin landscape. Here we show that genomic ablation of Smad ubiquitin regulatory factor 2 (Smurf2), a HECT-domain E3 ubiquitin ligase, results in dysregulation of both the DNA damage response and genomic stability, culminating in increased susceptibility to various types of cancers in aged mice. We show that Smurf2 regulates the monoubiquitination of histone H2B as well as the trimethylation of histone H3 at Lys4 and Lys79 by targeting ring finger protein 20 (RNF20) for proteasomal degradation in both mouse and human cells. We also show that Smurf2 and RNF20 are colocalized at the γ-H2AX foci of double-stranded DNA breaks in the nucleus. Thus, Smurf2 has a tumor suppression function that normally maintains genomic stability by controlling the epigenetic landscape of histone modifications through RNF20.


A tumor suppressor function of Smurf2 associated with controlling chromatin landscape and genome stability through RNF20. Blank M, Tang Y, Yamashita M, Burkett SS, Cheng SY, Zhang YE.  Nat Med. 2012 Jan 8;18(2):227-34.

Denatured collagens in Smurf2KO wound tissues

Smurf2 regulates inflammation and collagen processing in cutaneous wound healing through TGF-b/Smad3 signaling

Published Date

About the Cover:

Visualization of denatured collagen in Smurf2KO wound cross-section using the collagen hybridization peptide R-CHP. Denatured collagens can be observed in wound area but very little in the subdermal tissue around the wound after 14 days.


Wound healing is a highly conserved process that restores the integrity and functionality of injured tissues.  TGF-b is a master regulator of wound healing, whose signaling is attenuated by the E3 ubiquitin ligase Smurf2.  Here, the roles of Smurf2 in cutaneous wound healing were examined using a murine incisional cutaneous model.  We found that loss of Smurf2 increased early inflammation in the wounds and led to narrower wounds with greater breaking strength.  Loss of Smurf2 also led to more linearized collagen bundles in normal and wounded skin.  Gene expression analyses by RT-qPCR indicated that Smurf2-deficient fibroblasts had increased levels of TGF-b/Smad3 signaling and changes in expression profile of genes related to matrix turnover.  The effect of Smurf2 loss on wound healing and collagen bundling was attenuated by the heterozygous loss of Smad3.  Together, these results show that Smurf2 affects inflammation and collagen processing in cutaneous wounds by down-regulating TGF-b/Smad3 signaling.


Smurf2 regulates inflammation and collagen processing in cutaneous wound healing through TGF-b/Smad3 signaling. Stuelten CH, Melis N, Subramanian B, Tang Y, Kimicata M, Fisher JP, Weight R, Zhang YE.  Am J Pathol. 2022, Dec; 192(12):1699-1711.