Family 3 subject – LAD-III Lymphoblastoid Cell Line

The Family 3 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.

Contributors

Inventor Institute
Nancy Hogg Cancer Research UK, London Research Institute: Lincoln's Inn Fields
Cat. #: 153769
Unit size: 1×10^6 cells / vial
Cancer types: Blood cancer
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 Turkish subject that has Leukocyte Adhesion Deficiency-III (LAD-III) with a mutation in the kindlin-3 gene. LCLs are also available from the mother and father. This cell line was derived from 'Family 3 subject' as described in Svensson et al. 2009. N.Nat Med. 2009 Mar;15(3):306-12. PMID: 19234463. The Family 3 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.
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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