ResearcherUniversity of California San DiegoActive in the last 2 years
Ján Strnádel
Matched on ORCID iD 0000-0002-7233-6537; OpenAlex author ID A5068579790. Sources: OpenAlex.
Their work
- Papers
- 6 (first author 0, last author 1)
- Trials
- 0
- Grants
- 0
- Labs led
- 0
- Collaborators
- 19
2014: 1 paper · 2015: 1 paper · 2016: none · 2017: 1 paper · 2018: none · 2019: none · 2020: none · 2021: none · 2022: 1 paper · 2023: none · 2024: none · 2025: 1 paper · 2026: 1 paper
Papers 6
- Anti-Tumor Effects of Statins in Pancreatic Ductal Adenocarcinoma Cells. Co-author DOI 10.3390/ijms27072972↗
- Leveraging epigenetic alterations in pancreatic ductal adenocarcinoma for clinical applications. Co-author DOI 10.1016/j.semcancer.2025.01.003↗
- Establishment of PANDA - a new human pancreatic ductal adenocarcinoma cell line with 3D cell culture technology. Last author DOI 10.4149/210924n1360↗
- eIF5A-PEAK1 Signaling Regulates YAP1/TAZ Protein Expression and Pancreatic Cancer Cell Growth. Co-author DOI 10.1158/0008-5472.can-16-2594↗
- Eukaryotic Translation Initiation Factor 5A (EIF5A) Regulates Pancreatic Cancer Metastasis by Modulating RhoA and Rho-associated Kinase (ROCK) Protein Expressi… Co-author DOI 10.1074/jbc.m115.687418↗
- A hypusine-eIF5A-PEAK1 switch regulates the pathogenesis of pancreatic cancer. Co-author DOI 10.1158/0008-5472.can-14-1031↗
Closest collaborators
The 19 strongest of 19 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Erika Halášová · 2 shared papers, 2022–2026 · strength 0.37
- Veronika Kucháriková · 1 shared paper, 2026 · strength 0.26
- Michael Bouvet · 3 shared papers, 2014–2022 · strength 0.21
- Paper Establishment of PANDA - a new human pancreatic ductal adenocarcinoma cell line with 3D cell culture technology. DOI 10.4149/210924n1360↗
- Paper eIF5A-PEAK1 Signaling Regulates YAP1/TAZ Protein Expression and Pancreatic Cancer Cell Growth. DOI 10.1158/0008-5472.can-16-2594↗
- Paper A hypusine-eIF5A-PEAK1 switch regulates the pathogenesis of pancreatic cancer. DOI 10.1158/0008-5472.can-14-1031↗
- Chiara Corradi · 1 shared paper, 2025 · strength 0.19
- Verona Buociková · 1 shared paper, 2025 · strength 0.19
- Jörg Tost · 1 shared paper, 2025 · strength 0.19
- Seçil Ak Aksoy · 1 shared paper, 2025 · strength 0.19
- Riccardo Farinella · 1 shared paper, 2025 · strength 0.19
- Božena Smolková · 1 shared paper, 2025 · strength 0.19
- Maria Urbanova · 1 shared paper, 2025 · strength 0.19
- Daniele Campa · 1 shared paper, 2025 · strength 0.19
- Julie Earl · 1 shared paper, 2025 · strength 0.19
- Ken Fujimura · 3 shared papers, 2014–2017 · strength 0.16
- Paper Eukaryotic Translation Initiation Factor 5A (EIF5A) Regulates Pancreatic Cancer Metastasis by Modulating RhoA and Rho-a… DOI 10.1074/jbc.m115.687418↗
- Paper eIF5A-PEAK1 Signaling Regulates YAP1/TAZ Protein Expression and Pancreatic Cancer Cell Growth. DOI 10.1158/0008-5472.can-16-2594↗
- Paper A hypusine-eIF5A-PEAK1 switch regulates the pathogenesis of pancreatic cancer. DOI 10.1158/0008-5472.can-14-1031↗
- Richard L. Klemke · 3 shared papers, 2014–2017 · strength 0.16
- Paper Eukaryotic Translation Initiation Factor 5A (EIF5A) Regulates Pancreatic Cancer Metastasis by Modulating RhoA and Rho-a… DOI 10.1074/jbc.m115.687418↗
- Paper eIF5A-PEAK1 Signaling Regulates YAP1/TAZ Protein Expression and Pancreatic Cancer Cell Growth. DOI 10.1158/0008-5472.can-16-2594↗
- Paper A hypusine-eIF5A-PEAK1 switch regulates the pathogenesis of pancreatic cancer. DOI 10.1158/0008-5472.can-14-1031↗
- Romana Zahumenska · 1 shared paper, 2022 · strength 0.11
- Jonathan A. Kelber · 2 shared papers, 2014–2017 · strength 0.10
- Kun‐Liang Guan · 1 shared paper, 2017 · strength 0.06
- Cristina Angela Metildi · 1 shared paper, 2014 · strength 0.04
- Andrew M. Lowy · 1 shared paper, 2014 · strength 0.04
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.