Jin Yetao相关文献与解析，生知库 | 链接生命科学的每一步

Lu, Xiuju; Gibbs, James S; Hickman, Heather D; David, Alexandre; Dolan, Brian P; Jin, Yetao; Kranz, David M; Bennink, Jack R; Yewdell, Jonathan W; Varma, Rajat

微生物学

细胞生物学

发表日期：2012

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Hypoxia activates tumor suppressor p53 by inducing ATR-Chk1 kinase cascade-mediated phosphorylation and consequent 14-3-3γ inactivation of MDMX protein

缺氧通过诱导ATR-Chk1激酶级联介导的磷酸化激活肿瘤抑制因子p53，进而导致MDMX蛋白的14-3-3γ失活。

期刊:Journal of Biological Chemistry

影响因子:3.9

doi:10.1074/jbc.M111.336875

Lee, Jun-Ho; Jin, Yetao; He, Guifen; Zeng, Shelya X; Wang, Yunyuan V; Wahl, Geoffrey M; Lu, Hua

JTV1 co-activates FBP to induce USP29 transcription and stabilize p53 in response to oxidative stress

JTV1 与 FBP 协同激活，诱导 USP29 转录并稳定 p53，以应对氧化应激。

期刊:EMBO Journal

影响因子:8.3

doi:10.1038/emboj.2011.11

Liu, Juhong; Chung, Hye-Jung; Vogt, Matthew; Jin, Yetao; Malide, Daniela; He, Liusheng; Dundr, Miroslav; Levens, David

MDMX promotes proteasomal turnover of p21 at G1 and early S phases independently of, but in cooperation with, MDM2

MDMX 在 G1 期和早期 S 期促进 p21 的蛋白酶体降解，这一过程独立于 MDM2，但与 MDM2 协同作用。

期刊:Molecular and Cellular Biology

影响因子:2.7

doi:10.1128/MCB.01198-07

Jin, Yetao; Zeng, Shelya X; Sun, Xiao-Xin; Lee, Hunjoo; Blattner, Christine; Xiao, Zhixiong; Lu, Hua

MDM2

发表日期：2008

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SAG/ROC-SCF beta-TrCP E3 ubiquitin ligase promotes pro-caspase-3 degradation as a mechanism of apoptosis protection

SAG/ROC-SCF β-TrCP E3泛素连接酶促进pro-caspase-3降解，以此作为细胞凋亡保护机制。

期刊:Neoplasia

影响因子:7.7

doi:10.1593/neo.06568

Tan, Mingjia; Gallegos, Jayme R; Gu, Qingyang; Huang, Yuanhui; Li, Jun; Jin, Yetao; Lu, Hua; Sun, Yi

Balance of Yin and Yang: ubiquitylation-mediated regulation of p53 and c-Myc

阴阳平衡：泛素化介导的p53和c-Myc调控

期刊:Neoplasia

影响因子:7.7

doi:10.1593/neo.06334

Dai, Mu-Shui; Jin, Yetao; Gallegos, Jayme R; Lu, Hua

Ribosomal protein L23 activates p53 by inhibiting MDM2 function in response to ribosomal perturbation but not to translation inhibition.

核糖体蛋白 L23 通过抑制 MDM2 的功能来激活 p53，以应对核糖体扰动，但不会应对翻译抑制

期刊:Molecular and Cellular Biology

影响因子:2.7

doi:10.1128/MCB.24.17.7654-7668.2004

Dai Mu-Shui, Zeng Shelya X, Jin Yetao, Sun Xiao-Xin, David Larry, Lu Hua

Endogenous viral antigen processing generates peptide-specific MHC class I cell-surface clusters

内源性病毒抗原加工产生肽特异性MHC I类细胞表面簇

Hypoxia activates tumor suppressor p53 by inducing ATR-Chk1 kinase cascade-mediated phosphorylation and consequent 14-3-3γ inactivation of MDMX protein

缺氧通过诱导ATR-Chk1激酶级联介导的磷酸化激活肿瘤抑制因子p53，进而导致MDMX蛋白的14-3-3γ失活。

JTV1 co-activates FBP to induce USP29 transcription and stabilize p53 in response to oxidative stress

JTV1 与 FBP 协同激活，诱导 USP29 转录并稳定 p53，以应对氧化应激。

MDMX promotes proteasomal turnover of p21 at G1 and early S phases independently of, but in cooperation with, MDM2

MDMX 在 G1 期和早期 S 期促进 p21 的蛋白酶体降解，这一过程独立于 MDM2，但与 MDM2 协同作用。

SAG/ROC-SCF beta-TrCP E3 ubiquitin ligase promotes pro-caspase-3 degradation as a mechanism of apoptosis protection

SAG/ROC-SCF β-TrCP E3泛素连接酶促进pro-caspase-3降解，以此作为细胞凋亡保护机制。

Balance of Yin and Yang: ubiquitylation-mediated regulation of p53 and c-Myc

阴阳平衡：泛素化介导的p53和c-Myc调控

Ribosomal protein L23 activates p53 by inhibiting MDM2 function in response to ribosomal perturbation but not to translation inhibition.

核糖体蛋白 L23 通过抑制 MDM2 的功能来激活 p53，以应对核糖体扰动，但不会应对翻译抑制