WASF1 Knockout HEK293 Cell Line
Cat.No.:
EDJ-KQ6406
Species:
Human
Cell Name:
HEK293
Gene:
WASF1
Gene ID:
8936
Size:
1×10⁶cells
WASF1 Knockout Cell Line (HEK293) is an exclusive upgraded CRISPR/Cas9 system-mediated gene knockout cell, with the advantages of Optimized Strategy Design, Efficient Cell Transfection, High-Performance Cas9 Protein and Hassle-Free Cell Selection.
| Cat.No. | EDJ-KQ6406 |
|---|---|
| Product Name | WASF1 Knockout Cell Line(HEK 293) |
| Cell Line | HEK293 |
| Cellosaurus ID | CVCL_0045 |
| Cell Line Synonyms | Hek293, HEK-293, HEK/293, (HEK)293, HEK 293, HEK,293, 293, 293 HEK, 293 Ad5, Graham 293, Graham-293, Human Embryonic Kidney 293 |
| Gene | |
| NCBI Gene ID | |
| Gene Synonyms | NEDALVS|SCAR1|WAVE|WAVE-1|WAVE1 |
| Summary |
The protein encoded by this gene, a member of the Wiskott-Aldrich syndrome protein (WASP)-family, plays a critical role downstream of Rac, a Rho-family small GTPase, in regulating the actin cytoskeleton required for membrane ruffling. It has been shown to associate with an actin nucleation core Arp2/3 complex while enhancing actin polymerization in vitro. Wiskott-Aldrich syndrome is a disease of the immune system, likely due to defects in regulation of actin cytoskeleton. Multiple alternatively spliced transcript variants encoding the same protein have been found for this gene. [provided by RefSeq, Jul 2008]
|
| Associated Diseases | Non-tumor |
| Morphology | Adherent |
| Passage Ratio | 1/5，2days |
| Complete Culture Medium | DMEM + 10% FBS |
| Freezing Medium | 95% Complete culture medium+ 5% DMSO |
| QC | Indels validated by Sanger sequencing; sterility confirmed via microbial testing. |
* For research use only. Not intended for use in humans or animals, including clinical, therapeutic, or diagnostic purposes.
| Loci | STR Info (Sample Cell) Sample Cell Line: HEK293 | STR Info (Cell bank) Cell Line: HEK293 | ||
| Allele1 | Allele2 | Allele1 | Allele2 | |
| Amelogenin | X | X | ||
| CSF1P0 | 12 | 11 | 12 | |
| D2S1338 | 19 | 19 | ||
| D3S1358 | 15 | 17 | 15 | 17 |
| D5S818 | 8 | 8 | 9 | |
| D7S820 | 11 | 12 | 11 | 12 |
| D8S1179 | 12 | 14 | 12 | 14 |
| D13S317 | 12 | 14 | 12 | 14 |
| D16S539 | 9 | 13 | 9 | 13 |
| D18S51 | 17 | 18 | 17 | 18 |
| D19S433 | 15 | 18 | 15 | 18 |
| D21S11 | 28 | 30.2 | 28 | 30.2 |
| FGA | 23 | 23 | ||
| Penta D | 9 | 10 | 9 | 10 |
| Penta E | 7 | 15 | 7 | 15 |
| TH01 | 7 | 9.3 | 7 | 9.3 |
| TPOX | 11 | 11 | ||
| vWA | 16 | 19 | 16 | 19 |
| D6S1043 | 11 | 11 | ||
| D12S391 | 19 | 21 | 11 | 15 |
| D2S441 | 11 | 15 | 11 | 15 |
* STR authentication data of this cell line matches with that of cell lines sourced from ATCC, DSMZ, JCRB, and RIKEN databases.
Conclusion: The STR identification of this cell is correct.
Conclusion: The STR identification of this cell is correct.
* Research Use Disclaimer: Content is generated from publicly available research data, bioinformatic resources, and computational analyses for research reference only.
Research Publications
Nance-Horan Syndrome-like 1 protein negatively regulates Scar/WAVE-Arp2/3 activity and inhibits lamellipodia stability and cell migration.
IF=15.7
Nature communications
Cell migration is important for development and its aberrant regulation contributes to many diseases. The Scar/WAVE complex is essential for Arp2/3 mediated lamellipodia formation during mesenchymal cell migration and several coinciding signals activate it. However, so far, no direct negative regulators are known. Here we identify Nance-Horan Syndrome-like 1 protein (NHSL1) as a direct binding partner of the Scar/WAVE complex, which co-localise at protruding lamellipodia. This interaction is mediated by the Abi SH3 domain and two binding sites in NHSL1. Furthermore, active Rac binds to NHSL1 at two regions that mediate leading edge targeting of NHSL1. Surprisingly, NHSL1 inhibits cell migration through its interaction with the Scar/WAVE complex. Mechanistically, NHSL1 may reduce cell migration efficiency by impeding Arp2/3 activity, as measured in cells using a Arp2/3 FRET-FLIM biosensor, resulting in reduced F-actin density of lamellipodia, and consequently impairing the stability of lamellipodia protrusions.
This KO model may be useful for:
- Investigating the role of WASF1 in Scar/WAVE-Arp2/3 complex-mediated actin dynamics
- Studying lamellipodia stability and cell migration mechanisms
- Exploring the regulatory interplay between WASF1 and NHSL1 in cytoskeletal signaling
- Functional validation of WASF1 in cell motility and adhesion pathways
- Screening for modulators of actin nucleation and branching in migration-related assays
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