Jin Wu
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Jin Wu has a total of 105 co-authors. Here are the top co-authors by number of shared publications:
- Ailing Li
Nanhu Laboratory, National Center of Biomedical Analysis, Beijing, China
42 shared publications - Bohan Li
Department of Neurosurgery, Beijing Fengtai Hospital, Beijing, China. 5
42 shared publications - Cheng Zhang
Nanhu Laboratory, National Center of Biomedical Analysis, Beijing, China. 1
42 shared publications - Chenhui Wang
The Key Laboratory for Human Disease Gene Study of Sichuan Province and the Department of Laboratory Medicine, Sichuan Provincial People’s Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China
42 shared publications - Dake Xiao
College of traditional Chinese Medicine, Capital Medical University, Beijing, China
42 shared publications - Fangye Li
Department of Neurosurgery, First Medical Center of PLA General Hospital, Beijing, China. 6
42 shared publications
Latest Publications
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S6 from Phosphocreatine Promotes Epigenetic Reprogramming to Facilitate Glioblastoma Growth Through Stabilizing BRD2
Supplementary Table S6 shows the sequences of shRNAs used in this study.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S6 from Phosphocreatine Promotes Epigenetic Reprogramming to Facilitate Glioblastoma Growth Through Stabilizing BRD2
Supplementary Table S6 shows the sequences of shRNAs used in this study.
- Open Access
Quantum Dot-Based Dual-Fluorescence Aptasensing Platform Using Interface-Engineered MXene for Multiplex Protein Detection
Antigen detection provides rapid and convenient diagnosis of respiratory infections. This study develops an innovative dual-fluorescence aptasensing method based on polydopamine-functionalized MXene (PDA-MXene) for the simultaneous detection of spike protein and hemagglutinin protein. The method employs green- and red-emitting quantum dot (QD) probes as fluorescence reporters, and the PDA-MXene as an effective adsorption and separation substrate. Coupled with a centrifugation-assisted separation strategy, this design method reduces background interference and enhances detection reliability. The method demonstrates good analytical performance, with detection limits of 0.82 ng/mL for spike protein and 2.11 ng/mL for hemagglutinin protein in single-channel mode. The dual-channel mode enables reliable and simultaneous quantification of both target proteins with minimal spectral cross-talk. Furthermore, this method exhibits high specificity against interferents including ions, proteins, and toxins. Artificial saliva, chosen as real sample, is spiked with target proteins to investigate the practical applicability of the method, showing recovery rates for both target proteins between 100 and 114 sensing strategy is simple to operate and allows the detection of new targets by simply replacing the azide-modified aptamer lyophilized powder. It therefore holds promising application for the simultaneous detection of multiple proteins in point-of-care testing and health monitoring fields.
Open AccessQuantum Dot-Based Dual-Fluorescence Aptasensing Platform Using Interface-Engineered MXene for Multiplex Protein Detection
Antigen detection provides rapid and convenient diagnosis of respiratory infections. This study develops an innovative dual-fluorescence aptasensing method based on polydopamine-functionalized MXene (PDA-MXene) for the simultaneous detection of spike protein and hemagglutinin protein. The method employs green- and red-emitting quantum dot (QD) probes as fluorescence reporters, and the PDA-MXene as an effective adsorption and separation substrate. Coupled with a centrifugation-assisted separation strategy, this design method reduces background interference and enhances detection reliability. The method demonstrates good analytical performance, with detection limits of 0.82 ng/mL for spike protein and 2.11 ng/mL for hemagglutinin protein in single-channel mode. The dual-channel mode enables reliable and simultaneous quantification of both target proteins with minimal spectral cross-talk. Furthermore, this method exhibits high specificity against interferents including ions, proteins, and toxins. Artificial saliva, chosen as real sample, is spiked with target proteins to investigate the practical applicability of the method, showing recovery rates for both target proteins between 100 and 114 sensing strategy is simple to operate and allows the detection of new targets by simply replacing the azide-modified aptamer lyophilized powder. It therefore holds promising application for the simultaneous detection of multiple proteins in point-of-care testing and health monitoring fields.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S3 from Phosphocreatine Promotes Epigenetic Reprogramming to Facilitate Glioblastoma Growth Through Stabilizing BRD2
Supplementary Table S3 shows UCSC-predicted transcription factors that bind to CKB promoters.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S3 from Phosphocreatine Promotes Epigenetic Reprogramming to Facilitate Glioblastoma Growth Through Stabilizing BRD2
Supplementary Table S3 shows UCSC-predicted transcription factors that bind to CKB promoters.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S1 from Phosphocreatine Promotes Epigenetic Reprogramming to Facilitate Glioblastoma Growth Through Stabilizing BRD2
Supplementary Table S1 shows PCr IHC staining score in human glioma microarray.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S1 from Phosphocreatine Promotes Epigenetic Reprogramming to Facilitate Glioblastoma Growth Through Stabilizing BRD2
Supplementary Table S1 shows PCr IHC staining score in human glioma microarray.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S4 from Phosphocreatine Promotes Epigenetic Reprogramming to Facilitate Glioblastoma Growth Through Stabilizing BRD2
Supplementary Table S4 shows PCr and BRD2 IHC staining scores in the serial sections of human glioma microarrays.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S4 from Phosphocreatine Promotes Epigenetic Reprogramming to Facilitate Glioblastoma Growth Through Stabilizing BRD2
Supplementary Table S4 shows PCr and BRD2 IHC staining scores in the serial sections of human glioma microarrays.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Figures S1-S8 from Phosphocreatine Promotes Epigenetic Reprogramming to Facilitate Glioblastoma Growth Through Stabilizing BRD2
Supplementary Figures S1 shows that GSCs produce high levels of phosphocreatine through upregulating CKB. Supplementary Figures S2 shows that ZEB1 promotes CKB transcription in GSCs. Supplementary Figures S3 shows that knockdown of CKB impedes GBM growth. Supplementary Figures S4 shows that disruption of phosphocreatine production impedes GBM growth. Supplementary Figures S5 shows that cCr treatment shows no side effect on mice. Supplementary Figures S6 shows that phosphocreatine binds to BRD2 and inhibits its ubiquitin mediated proteasomal degradation. Supplementary Figures S7 shows that phosphocreatine promotes chromosome segregation and GSC proliferation through BRD2 mediated transcription. Supplementary Figures S8 shows that disruption of phosphocreatine biosynthesis by cCr improves JQ1 therapeutic efficacy in GBM.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Figures S1-S8 from Phosphocreatine Promotes Epigenetic Reprogramming to Facilitate Glioblastoma Growth Through Stabilizing BRD2
Supplementary Figures S1 shows that GSCs produce high levels of phosphocreatine through upregulating CKB. Supplementary Figures S2 shows that ZEB1 promotes CKB transcription in GSCs. Supplementary Figures S3 shows that knockdown of CKB impedes GBM growth. Supplementary Figures S4 shows that disruption of phosphocreatine production impedes GBM growth. Supplementary Figures S5 shows that cCr treatment shows no side effect on mice. Supplementary Figures S6 shows that phosphocreatine binds to BRD2 and inhibits its ubiquitin mediated proteasomal degradation. Supplementary Figures S7 shows that phosphocreatine promotes chromosome segregation and GSC proliferation through BRD2 mediated transcription. Supplementary Figures S8 shows that disruption of phosphocreatine biosynthesis by cCr improves JQ1 therapeutic efficacy in GBM.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S5 from Phosphocreatine Promotes Epigenetic Reprogramming to Facilitate Glioblastoma Growth Through Stabilizing BRD2
Supplementary Table S5 shows the detailed genetic mutations of four GBM cell lines.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S5 from Phosphocreatine Promotes Epigenetic Reprogramming to Facilitate Glioblastoma Growth Through Stabilizing BRD2
Supplementary Table S5 shows the detailed genetic mutations of four GBM cell lines.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S2 from Phosphocreatine Promotes Epigenetic Reprogramming to Facilitate Glioblastoma Growth Through Stabilizing BRD2
Supplementary Table S2 shows CKB IHC staining score in human glioma microarray.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S2 from Phosphocreatine Promotes Epigenetic Reprogramming to Facilitate Glioblastoma Growth Through Stabilizing BRD2
Supplementary Table S2 shows CKB IHC staining score in human glioma microarray.
- Open Access
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Supplementary Table S7 from Phosphocreatine Promotes Epigenetic Reprogramming to Facilitate Glioblastoma Growth Through Stabilizing BRD2
Supplementary Table S7 shows the primer sequences used for Real-Time PCR.
- 17 June 2026
- Published by American Association for Cancer Research (AACR)
Open AccessSupplementary Table S7 from Phosphocreatine Promotes Epigenetic Reprogramming to Facilitate Glioblastoma Growth Through Stabilizing BRD2
Supplementary Table S7 shows the primer sequences used for Real-Time PCR.
- 2 April 2026
- Published by Elsevier in Spectrochimica Acta Part A: Molecular and Biomolecular Spectroscopy
- Vol. 358, 127848
Dual-mode manganese dioxide nanosheets and nitrogen-doped molybdenum oxide quantum dots-based smartphone-assisted ratiometric fluorescence probe for butyrylcholinesterase and malachite green detection
- 2 April 2026
- Published by Elsevier in Spectrochimica Acta Part A: Molecular and Biomolecular Spectroscopy
- Vol. 358, 127848
Dual-mode manganese dioxide nanosheets and nitrogen-doped molybdenum oxide quantum dots-based smartphone-assisted ratiometric fluorescence probe for butyrylcholinesterase and malachite green detection