王雅既不承认也不否认 ORI 的研究不当行为调查结果。双方签订了自愿排除协议以结束此事，而无需进一步花费时间、财务或其他资源。
ORI 发现，王雅故意、有意和/或伪造以下一 (1) 份 PHS 拨款申请和六 (6) 篇已发表论文中的数据，从事研究不端行为：
R21 HL154577-01, “GPRC5A Inhibits Error-Prone Repair to Maintain Lung Genomic Integrity,” submitted to the National Heart, Lung, and Blood Institute (NHLBI), NIH, on December 13, 2019.
miR-21-Mediated Radioresistance Occurs via Promoting Repair of DNA Double Strand Breaks. J Biol Chem. 2017 Feb 24;292(8):3531-40; doi: 10.1074/jbc.M116.772392 (hereafter referred to as “J Biol Chem. 2017”). Retraction in: J Biol Chem. 2020 May 1;295(18):6250; doi: 10.1074/jbc.W120.013725.
Distinct Roles of Ape1 Protein, an Enzyme Involved in DNA Repair, in High or Low Linear Energy Transfer Ionizing Radiation-Induced Cell Killing. J Biol Chem. 2014 Oct 31; 289(44):30635-44; doi: 10.1074/jbc.M114.604959 (hereafter referred to as “J Biol Chem. 2014”). Retraction in: J Biol Chem. 2020 May 1;295(18):6249; doi: 10.1074/jbc.W120.013724.
OCT4 as a Target of miR-34a Stimulates p63 but Inhibits p53 to Promote Human Cell Transformation. Cell Death Dis. 2014 Jan 23;5(1):e1024; doi: 10.1038/cddis.2013.563 (hereafter referred to as “Cell Death Dis. 2014”).
MicroRNA-21 Modulates the Levels of Reactive Oxygen Species by Targeting SOD3 and TNFα. Cancer Res. 2012 Sep 15;72(18):4707-13; doi: 10.1158/0008-5472.CAN-12-0639 (hereafter referred to as “Cancer Res. 2012a”).
RNAi-Mediated Targeting of Noncoding and Coding Sequences in DNA Repair Gene Messages Efficiently Radiosensitizes Human Tumor Cells. Cancer Res. 2012 Mar 1; 72(5):1221-8; doi: 10.1158/0008-5472.CAN-11-2785 (hereafter referred to as “Cancer Res. 2012b”).
Over-Expression of miR-100 is Responsible for the Low-Expression of ATM in the Human Glioma Cell Line: M059J. DNA Repair (Amst). 2010 Nov 10;9(11):1170-5; doi: 10.1016/j.dnarep.2010.08.007 (hereafter referred to as “DNA Repair 2010”).
ORI 发现王雅通过重复使用和重新标记相同的图像来代表 DNA 损伤和修复的哺乳动物组织培养模型中的不同实验条件图像，故意、有意和/或无意伪造蛋白质免疫印迹数据。
Figure 3D in J Biol Chem. 2017, representing β-actin expression (left side panel) in wildtype (WT), microRNA-21 (miR-21) knock-in, and miR-21-/- mouse embryonic fibroblast (MEF) cells exposed to irradiation
Figure 4C in J Biol Chem. 2017, representing DNA-PKcs expression in miR-21 knock-in MEF cells exposed to irradiation
Figure 5A in J Biol Chem. 2017, representing CDC25A and β-actin expression in WT, GSK3B-/-, and Cyclin D1-/- MEF cells transfected with control or gene-specific silencing RNA (siRNA)
Figure 1 in J Biol Chem. 2014, representing β-actin expression in Ku80-/- (Figure 1A) and Ogg1-/- (Figure 1C) MEF cells transfected with expression or control vectors
Figure 3 in J Biol Chem. 2014, representing H2A expression in WT MEF (Figure 3A), Ku80-/- MEF (Figure 3B), Ogg1-/- MEF (Figure 3C), and Ogg1+ (rescue) MEF (Figure 3D) cells transfected with expression or control vectors and in the absence or presence of radiation exposure
Figure 3D in J Biol Chem. 2014, representing Mre11 (left panel) expression in Ogg1+ (rescue) MEF cells transfected with expression or control vectors in the absence or presence of radiation exposure
Figure 4B in J Biol Chem. 2014, representing Mre11 expression in Ogg1-/- MEFcells with control or Ape1 expression vector in the presence of low or high linear energy transfer (LET) irradiation
Figure 5C in J Biol Chem. 2014, representing Ape1 and β-actin expression in WT MEF cells with or without gene depletion and transfected with control or various Ape1 expression vectors
Figure 4A in NIH grant application R21 HL154577-01, representing GPRC5A levels in different patient-derived cell lines with gene suppression or depletion
Figure 4D in J Biol Chem. 2017, representing total DNA-PKcs, phosphorylated DNA-PKcs, CDC25A, and GSK3B levels in human embryonic kidney cells transfected with controls or various expression vectors and/or miR-21 mimics
Figure 5C in J Biol Chem. 2017, representing CDC25A, GSK3B, Cyclin D1, and β-actin expression in human embryonic kidney cells with or without gene depletion and transfected with controls or miR-21 mimics
Figure 5B in Cell Death Dis. 2014, representing p53 and p63 levels in human lung epithelial cells with or without gene depletion
Figure 3A in Cancer Res. 2012a, representing TNFα levels in control and miR-21 overexpressing human lung epithelial cells at different time points following irradiation
Figure 5A in Cancer Res. 2012b, representing XRCC4 levels in both human lung and brain epithelial cells with gene depletion at multiple time points and treated with or without an artificial microRNA
Figure 3A in DNA Repair 2010, representing ATM and Ku70 levels in human glioblastoma-derived cells with or without gene depletion
来自用对照或表达载体转染的小鼠细胞系中染色质 DNA 复合物的蛋白质的蛋白质印迹图像，在不存在或存在照射的情况下通过重复使用免疫印迹条带并重新标记它们以代表1篇文章三 (3) 个图形面板，包括：
Figure 3 in J Biol Chem. 2014, representing chromatin-bound γ-H2AX levels in WT MEF (Figure 3A), Ogg1-/- MEF (Figure 3C), and Ogg1+ (rescue) MEF (Figure 3D) cells transfected with a control or expression vector and in the absence or presence of irradiation
Respondent agreed to exclude herself voluntarily for a period of four (4) years beginning on August 4, 2021, from any contracting or subcontracting with any agency of the United States Government and from eligibility for or involvement in nonprocurement programs of the United States Government referred to as “covered transactions” pursuant to HHS’ Implementation (2 C.F.R. Part 376) of OMB Guidelines to Agencies on Governmentwide Debarment and Suspension, 2 C.F.R. Part 180 (collectively the “Debarment Regulations”).
Respondent agreed to exclude herself voluntarily from serving in any advisory capacity to PHS including, but not limited to, service on any PHS advisory committee, board, and/or peer review committee, or as a consultant for a period of four (4) years, beginning on August 4, 2021.
As a condition of the Agreement, Respondent will request that the following papers be corrected or retracted in accordance with 42 C.F.R. § 93.407(a)(1) and § 93.411(b):