Family 1 subject – LAD-III Lymphoblastoid Cell Line

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.

Contributors

Inventor Institute
Nancy Hogg Cancer Research UK, London Research Institute: Lincoln's Inn Fields
Cat. #: 153766
Unit size: 1×10^6 cells / vial
Research Fields: Cell biology;Immunology
Organism: Human
Tissue: Blood
Growth properties: Suspension, lymphoblastoid cell line
Cancer Types In Detail: Leukocyte Adhesion Deficiency-III (LAD-III)
Alternate name: Fermitin family homolog 3, MIG2-like protein, Unc-112-related protein 2
Product 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.
Disease: Cancer
Format: Frozen
Storage conditions: Liquid Nitrogen
Shipping conditions: Dry ice
Growth medium: RPMI-1640 + 10% FCS
Mycoplasma free: Yes
Biosafety level: 1
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.

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