- decreased thymocyte number / MGI
- exencephaly / MGI
- open neural tube / MGI
- decreased IgG level / MGI
- decreased IgM level / MGI
- abnormal immune cell physiology / MGI
- abnormal T cell activation / MGI
- decreased activated T cell number / MGI
- abnormal T cell differentiation / MGI
- abnormal dendritic cell physiology / MGI
- increased susceptibility to infection / MGI
- decreased immunoglobulin level / MGI
- abnormal neural fold elevation formation / MGI
- abnormal response to infection / MGI
- abnormal cytotoxic T cell physiology / MGI
- increased double-negative T cell number / MGI
- decreased double-positive T cell number / MGI
- decreased B cell proliferation / MGI
- decreased T cell proliferation / MGI
- cellular phenotype / MGI
- perinatal lethality, incomplete penetrance / MGI
- increased hindbrain apoptosis / MGI
B6.129P2-Bcl10tm1Mak/Cnbc
Status | Available to order |
EMMA ID | EM:06383 |
International strain name | B6.129P2-Bcl10tm1Mak/Cnbc |
Alternative name | Bcl10 |
Strain type | Targeted Mutant Strains : Knock-out |
Allele/Transgene symbol | Bcl10tm1Mak |
Gene/Transgene symbol | Bcl10 |
Information from provider
Provider | Tak W Mak |
Provider affiliation | Mak Lab, Campbell Family Breast Cancer reseach Institute |
Genetic information | A targeting vector was designed to replace exon 2 and the complete coding sequence of exon 3 with a neomycin resistance gene cassette (neo) in antisense orientation. |
Phenotypic information | Heterozygous (+/-) mice were healthy up to nine months of age and intercrossed to obtain homozygous Bcl10 deficient mutants (-/-). Of 372 offspring from heterozygous intercrosses, only 65 (17.5%) homozygous mutants were identified, indicating that about one third of Bcl10-/- mutants died during embryogenesis. Bcl10-/- mutants that survived embryonic development were fertile, did not show any gross anatomical abnormalities, and did not develop any malignancies up to 6 months of age. Bcl10 deficiency results in partial embryonic lethality caused by a neural tube closure defect. |
Breeding history | Backcrossed 10 times to C57BL/6. |
References |
|
Homozygous fertile | no |
Homozygous viable | no |
Homozygous matings required | no |
Immunocompromised | no |
Information from EMMA
Archiving centre | CNB-CSIC, Centro Nacional de Biotecnologia, Madrid, Spain |
Animals used for archiving | homozygous C57BL/6J |
Disease and phenotype information
MGI phenotypes (allele matching)
MGI phenotypes (gene matching)
- decreased thymocyte number / MGI
- exencephaly / MGI
- open neural tube / MGI
- abnormal humoral immune response / MGI
- decreased IgG level / MGI
- decreased IgM level / MGI
- abnormal immune cell physiology / MGI
- abnormal T cell activation / MGI
- decreased activated T cell number / MGI
- abnormal B cell differentiation / MGI
- abnormal T cell differentiation / MGI
- abnormal dendritic cell physiology / MGI
- increased susceptibility to infection / MGI
- increased susceptibility to bacterial infection / MGI
- decreased immunoglobulin level / MGI
- increased IgM level / MGI
- increased IgE level / MGI
- abnormal cytokine secretion / MGI
- abnormal neural fold elevation formation / MGI
- decreased B-1 B cell number / MGI
- increased T cell number / MGI
- decreased B cell number / MGI
- abnormal response to infection / MGI
- abnormal cytotoxic T cell physiology / MGI
- increased double-negative T cell number / MGI
- decreased double-positive T cell number / MGI
- decreased B cell proliferation / MGI
- decreased T cell proliferation / MGI
- cellular phenotype / MGI
- increased CD4-positive, alpha beta T cell number / MGI
- increased single-positive T cell number / MGI
- decreased follicular B cell number / MGI
- decreased marginal zone B cell number / MGI
- abnormal marginal zone B cell physiology / MGI
- decreased mature B cell number / MGI
- perinatal lethality, incomplete penetrance / MGI
- increased hindbrain apoptosis / MGI
Literature references
- Bcl10 is a positive regulator of antigen receptor-induced activation of NF-kappaB and neural tube closure.;Ruland J, Duncan G S, Elia A, del Barco Barrantes I, Nguyen L, Plyte S, Millar D G, Bouchard D, Wakeham A, Ohashi P S, Mak T W, ;2001;Cell;104;33-42; 11163238
- Bcl10/Malt1 signaling is essential for TCR-induced NF-kappaB activation in thymocytes but dispensable for positive or negative selection.;Jost Philipp J, Weiss Stephanie, Ferch Uta, Gross Olaf, Mak Tak W, Peschel Christian, Ruland Jürgen, ;2007;Journal of immunology (Baltimore, Md. : 1950);178;953-60; 17202357
Information on how we integrate external resources can be found here
INFRAFRONTIER® and European Mouse Mutant Archive - EMMA® are registered trademarks at the European Union Intellectual Property Office (EUIPO).