ResearcherShandong Normal UniversityNo recent work listed
Min Liu
Matched on ORCID iD 0000-0002-1626-7100; OpenAlex author ID A5100343883. Sources: OpenAlex.
Their work
- Papers
- 7 (first author 0, last author 2)
- Trials
- 0
- Grants
- 0
- Labs led
- 1
- Collaborators
- 8
2011: 1 paper · 2012: 1 paper · 2013: 1 paper · 2014: none · 2015: none · 2016: 2 papers · 2017: 1 paper · 2018: none · 2019: 1 paper
Papers 7
- CYLD deficiency promotes pancreatic cancer development by causing mitotic defects. Last author DOI 10.1002/jcp.27658↗
- EB1 phosphorylation mediates the functions of ASK1 in pancreatic cancer development. Co-author DOI 10.18632/oncotarget.21004↗
- Cep70 overexpression stimulates pancreatic cancer by inducing centrosome abnormality and microtubule disorganization. Last author DOI 10.1038/srep21263↗
- Apoptosis signal-regulating kinase 1 exhibits oncogenic activity in pancreatic cancer. Co-author DOI 10.18632/oncotarget.12090↗
- Histone deacetylase 6 and cytoplasmic linker protein 170 function together to regulate the motility of pancreatic cancer cells. Co-author DOI 10.1007/s13238-013-0010-3↗
- Validation of Polo-like kinase 1 as a therapeutic target in pancreatic cancer cells. Co-author DOI 10.4161/cbt.21412↗
- Dimethylenastron suppresses human pancreatic cancer cell migration and invasion in vitro via allosteric inhibition of mitotic kinesin Eg5. Co-author DOI 10.1038/aps.2011.130↗
Closest collaborators
The 8 strongest of 8 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Jun Zhou · 7 shared papers, 2011–2019 · strength 0.38
- Paper CYLD deficiency promotes pancreatic cancer development by causing mitotic defects. DOI 10.1002/jcp.27658↗
- Paper EB1 phosphorylation mediates the functions of ASK1 in pancreatic cancer development. DOI 10.18632/oncotarget.21004↗
- Paper Apoptosis signal-regulating kinase 1 exhibits oncogenic activity in pancreatic cancer. DOI 10.18632/oncotarget.12090↗
- Dengwen Li · 6 shared papers, 2012–2019 · strength 0.36
- Paper CYLD deficiency promotes pancreatic cancer development by causing mitotic defects. DOI 10.1002/jcp.27658↗
- Paper EB1 phosphorylation mediates the functions of ASK1 in pancreatic cancer development. DOI 10.18632/oncotarget.21004↗
- Paper Apoptosis signal-regulating kinase 1 exhibits oncogenic activity in pancreatic cancer. DOI 10.18632/oncotarget.12090↗
- Songbo Xie · 4 shared papers, 2013–2019 · strength 0.25
- Paper CYLD deficiency promotes pancreatic cancer development by causing mitotic defects. DOI 10.1002/jcp.27658↗
- Paper Apoptosis signal-regulating kinase 1 exhibits oncogenic activity in pancreatic cancer. DOI 10.18632/oncotarget.12090↗
- Paper Cep70 overexpression stimulates pancreatic cancer by inducing centrosome abnormality and microtubule disorganization. DOI 10.1038/srep21263↗
- Youguang Luo · 3 shared papers, 2011–2017 · strength 0.16
- Paper EB1 phosphorylation mediates the functions of ASK1 in pancreatic cancer development. DOI 10.18632/oncotarget.21004↗
- Paper Apoptosis signal-regulating kinase 1 exhibits oncogenic activity in pancreatic cancer. DOI 10.18632/oncotarget.12090↗
- Paper Dimethylenastron suppresses human pancreatic cancer cell migration and invasion in vitro via allosteric inhibition of m… DOI 10.1038/aps.2011.130↗
- Siqi Gao · 2 shared papers, 2016–2017 · strength 0.13
- Xiaodong Sun · 3 shared papers, 2011–2013 · strength 0.10
- Paper Histone deacetylase 6 and cytoplasmic linker protein 170 function together to regulate the motility of pancreatic cance… DOI 10.1007/s13238-013-0010-3↗
- Paper Validation of Polo-like kinase 1 as a therapeutic target in pancreatic cancer cells. DOI 10.4161/cbt.21412↗
- Paper Dimethylenastron suppresses human pancreatic cancer cell migration and invasion in vitro via allosteric inhibition of m… DOI 10.1038/aps.2011.130↗
- Shiyu Liu · 1 shared paper, 2016 · strength 0.06
- Chao Zhang · 1 shared paper, 2012 · strength 0.03
How to reach this person
A chain of introductions through people who have published, run trials or held grants together (warm_path@1: fewest links first, then the strongest). Built from public records only; no contact details are kept.