Cat. #153767
Family 2 subject – LAD-III EBV Lymphoblastoid Cell Line
Cat. #: 153767
Unit size: 1x10^6 cells / vial
Availability: 8-10 weeks
Organism: Human
Tissue: Blood
Disease: Cancer
£575.00
This fee is applicable only for non-profit organisations. If you are a for-profit organisation or a researcher working on commercially-sponsored academic research, you will need to contact our licensing team for a commercial use license.
Contributor
Inventor: Nancy Hogg
Institute: Cancer Research UK, London Research Institute: Lincoln's Inn Fields
Tool Details
*FOR RESEARCH USE ONLY (for other uses, please contact the licensing team)
- Name: Family 2 subject – LAD-III EBV Lymphoblastoid Cell Line
- Alternate name: Fermitin family homolog 3, MIG2-like protein, Unc-112-related protein 2
- Cancer: Blood cancer
- Cancers detailed: Leukocyte Adhesion Deficiency-III (LAD-III)
- Research fields: Cell biology;Immunology
- Organism: Human
- Tissue: Blood
- Disease: Cancer
- Growth properties: Suspension, lymphoblastoid cell line
- Description: An EBV-transformed B lymphoblastoid cell line (LCL) derived from a Turkish subject that has Leukocyte Adhesion Deficiency-III (LAD-III) with a mutation in the kindlin-3 gene. LCLs are also available from the father. This cell line was derived from 'Family 2 subject' as described in Svensson et al. 2009. N.Nat Med. 2009 Mar;15(3):306-12. PMID: 19234463. The Family 2 subject has an inactivating mutation in exon 12 of the KINDLIN3 gene resulting in a translational stop codon. This mutation leads to an overall decrease in KINDLIN3 mRNA levels and loss of protein expression.
- Biosafety level: 1
Target Details
- Target: Kindlin-3, UniProt ID:Q86UX7
Handling
- Format: Frozen
- Growth medium: RPMI-1640 + 10% FCS
- Unit size: 1x10^6 cells / vial
- Shipping conditions: Dry ice
- Storage conditions: Liquid Nitrogen
- Mycoplasma free: Yes
Related Tools
- Related tools: Family 2 father - LAD-III EBV Lymphoblastoid Cell Line
References
- Svensson et al. 2009. Nat Med. 15(3):306-12. PMID: 19234463.
- Leukocyte adhesion deficiency-III is caused by mutations in KINDLIN3 affecting integrin activation.
