- hypoplasia / IMPC
- abnormal embryo size / IMPC
- preweaning lethality, incomplete penetrance / IMPC
- developmental dysplasia / IMPC
- decreased body length / IMPC
- edema / IMPC
- female infertility / IMPC
- microphthalmia / IMPC
- male infertility / IMPC
- increased mean corpuscular volume / IMPC
- abnormal cranium morphology / IMPC
STOCK Cdk4tm2.1Bbd/Cnbc
Status | Available to order |
EMMA ID | EM:08029 |
International strain name | STOCK Cdk4tm2.1Bbd/Cnbc |
Alternative name | Cdk4 |
Strain type | Targeted Mutant Strains : Knock-out |
Allele/Transgene symbol | Cdk4tm2.1Bbd |
Gene/Transgene symbol | Cdk4 |
Information from provider
Provider | Mariano Barbacid |
Provider affiliation | Molecular Oncology, Centro Nacional de Investigaciones Oncologicas |
Genetic information | An frt site was inserted 230 bp upstream of exon 2 and a PGK-hygromycin cassette flanked by frt sites was inserted 115 bp downstream of exon 4. The PGK-hygromycin cassette and exons 2-4 of Cdk4 were excised by Flp-mediated recombination. This is the resulting knock-out mouse line, after frt-mediated exon excision. |
Phenotypic information | Homozygous:Flp-mediated excision of exons 2-4 creates a null allele for Cdk4. Homozygous mice for the null allele have smaller size, noticeable at birth and progressively more noticeable with age. Mice develop diabetes after 2 months of age due to a drastic reduction in pancreatic beta cell numbers and islet size. Complete infertility in females and partial infertility in males is also observed. Reduction in pituitary gland size and pituitary-hormones production.Heterozygous:Heterozygous mice are viable |
Breeding history | Chimeras were crossed with CD1 females for germ line transmission analysis. Heterozygous animals for the three-frt sites allele were crossed with transgenic CAG-Flp mice to excise the frt-PGKneo-frt cassette and exons 2-4 of Cdk4. Line was maintained by inter-crossing heterozygous animals for the Cdk4 null allele. Genetic background involves 129S1/Sv, 129X1/SvJ, CD1 and C57BL/6J. |
References |
|
Homozygous fertile | no |
Homozygous viable | yes |
Homozygous matings required | no |
Immunocompromised | no |
Information from EMMA
Archiving centre | CNB-CSIC, Centro Nacional de Biotecnologia, Madrid, Spain |
Animals used for archiving | heterozygous C57BL/6J |
Disease and phenotype information
IMPC phenotypes (gene matching)
MGI phenotypes (gene matching)
- abnormal female reproductive system morphology / MGI
- small ovary / MGI
- abnormal male reproductive system morphology / MGI
- abnormal testis morphology / MGI
- small testis / MGI
- Leydig cell hyperplasia / MGI
- small seminiferous tubules / MGI
- increased body weight / MGI
- decreased body weight / MGI
- decreased body size / MGI
- abnormal locomotor behavior / MGI
- hyperactivity / MGI
- polydipsia / MGI
- impaired limb coordination / MGI
- hyperglycemia / MGI
- increased urine glucose level / MGI
- polyuria / MGI
- reduced male fertility / MGI
- male infertility / MGI
- female infertility / MGI
- abnormal glucose homeostasis / MGI
- postnatal lethality / MGI
- abnormal fertility/fecundity / MGI
- no abnormal phenotype detected / MGI
- abnormal seminiferous tubule morphology / MGI
- abnormal corpus luteum morphology / MGI
- oligozoospermia / MGI
- decreased circulating insulin level / MGI
- abnormal Sertoli cell morphology / MGI
- absent Leydig cells / MGI
- decreased circulating follicle stimulating hormone level / MGI
- ketoaciduria / MGI
- abnormal cell cycle / MGI
- impaired luteinization / MGI
- increased pancreatic beta cell number / MGI
- abnormal male reproductive system physiology / MGI
- abnormal female reproductive system physiology / MGI
- decreased testis weight / MGI
- azoospermia / MGI
- decreased circulating progesterone level / MGI
- abnormal pancreatic islet morphology / MGI
- homeostasis/metabolism phenotype / MGI
- Leydig cell hypoplasia / MGI
- decreased lactotroph cell number / MGI
- adenohypophysis hypoplasia / MGI
- delayed estrous cycle / MGI
- small pancreatic islets / MGI
- postnatal lethality, incomplete penetrance / MGI
Literature references
- Mice thrive without Cdk4 and Cdk2.;Barrière Cédric, Santamaría David, Cerqueira Antonio, Galán Javier, Martín Alberto, Ortega Sagrario, Malumbres Marcos, Dubus Pierre, Barbacid Mariano, ;2007;Molecular oncology;1;72-83; 19383288
- A synthetic lethal interaction between K-Ras oncogenes and Cdk4 unveils a therapeutic strategy for non-small cell lung carcinoma.;Puyol Marta, Martín Alberto, Dubus Pierre, Mulero Francisca, Pizcueta Pilar, Khan Gulfaraz, Guerra Carmen, Santamaría David, Barbacid Mariano, ;2010;Cancer cell;18;63-73; 20609353
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