Cat. #153766
Family 1 subject – LAD-III Lymphoblastoid Cell Line
Cat. #: 153766
Unit size: 1x10^6 cells / vial
Availability: 3-4 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
- Name: Family 1 subject – LAD-III Lymphoblastoid Cell Line
- Alternate name: Fermitin family homolog 3, MIG2-like protein, Unc-112-related protein 2
- Organism: Human
- Tissue: Blood
- Disease: Cancer
- Growth properties: Suspension, lymphoblastoid cell line
- Description: An EBV-transformed B lymphoblastoid cell line (LCL) derived from a Maltese subject that has Leukocyte Adhesion Deficiency-III (LAD-III) with a mutation in the kindlin-3 gene. LCLs are also available from the mother, father and sister. This cell line was derived from 'Family 1 subject' as described in Svensson et al. 2009. N.Nat Med. 2009 Mar;15(3):306-12. PMID: 19234463. The Family 1 subject has a homozygous inactivating mutation within the splice acceptor site of exon 14 in the KINDLIN3 gene. 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 1 father - LAD-III Lymphoblastoid Cell Line ; Family 1 mother - LAD-III Lymphoblastoid Cell Line ; Family 1 sibling - LAD-III 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.
