Abstract
The HECT domain E3 ubiquitin ligase SMURF2 regulates stability of several key protein targets involved in tumorigenesis, cell proliferation, migration, differentiation, and senescence. While altered levels and aberrant cellular distribution of SMURF2 were reported in different types of cancer, its role in tumorigenesis is far from understood. To elucidate the role of SMURF2 in cancer, appropriate human cancer cell models are needed. Here, we describe approaches that can be used to generate human normal and cancer cell strains knocked-out for SMURF2 using the clustered regularly interspaced short palindromic repeats (CRISPR/Cas9) gene-editing technology.
Original language | English |
---|---|
Pages (from-to) | 56-59 |
Number of pages | 4 |
Journal | Analytical Biochemistry |
Volume | 531 |
DOIs | |
State | Published - 15 Aug 2017 |
Bibliographical note
Publisher Copyright:© 2017 Elsevier Inc.
Funding
This work was supported by the ICRF (grant number 00636), Marie-Curie FP-7 CIG (grant number 612816), the Israel Cancer Association (grant numbers 20160073 and 20171153), and Dayan Family Foundation (to M.B); and by the Israel Science Foundation (grant number 996/12), the Israel Cancer Association (grant number 20141043) and ICRF (grant number 12-709-RCDA) (to H.G.H.).
Funders | Funder number |
---|---|
Dayan Family Foundation | |
Marie-Curie FP-7 CIG | 612816 |
Israel Cancer Research Fund | 00636 |
Israel Cancer Association | 20171153, 20160073 |
Israel Science Foundation | 12-709-RCDA, 20141043, 996/12 |
Keywords
- CRISPR/Cas9
- Human cells
- Knockout
- SMURF2