Strain Name:

B6;129S2-Bcl2tm1Sjk/J

Stock Number:

002265

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Availability:

Cryopreserved - Ready for recovery

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Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Mutant Stock; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Specieslaboratory mouse
 
Donating InvestigatorDr. Stanley J. Korsmeyer,   Dana-Farber Cancer Institute

Appearance
black
Related Genotype: a/a

Description
Mice homozygous for the Bcl2tm1Sjk targeted mutation appear normal at birth; however, growth retardation is evident by one week of age with considerable heterogeneity in weight compared to normal wildtype siblings (30% to 90%). There is some pre-weaning loss. Homozygotes succumb to renal failure as a result of polycystic kidney disease. Hematopoiesis, including lymphocyte differentiation is initially normal but the thymus and spleen decrease in size due to increased apoptosis. The coat color of homozygotes turns grey with the second hair follicle cycle.

Control Information

  Control
   Wild-type from the colony
   101045 B6129SF2/J (approximate)
 
  Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Bcl2
003082   129S1/SvImJ-Bcl2tm1Mpin/J
018430   B6.129X1(Cg)-Bcl2tm1.1Sjk/J
003069   B6.NOD-(D1Mit3-Bcl2) (D17Mit21-D17Mit10)/LtJ
003062   B6.NOD-(D1Mit3-Bcl2)/J
008882   STOCK Bcl2tm1Irt/J
View Strains carrying other alleles of Bcl2     (5 strains)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
B-Cell Cll/Lymphoma 2; BCL2   (BCL2)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Bcl2tm1Sjk/Bcl2tm1Sjk

        involves: 129S2/SvPas * C57BL/6
  • mortality/aging
  • partial postnatal lethality
    • the smallest mutants become noticeably ill and die after 1 week of age, however, the onset of morbidity has a wide range (10 days to 10 weeks), although there is a clustering at 2-3 weeks, just prior to weaning   (MGI Ref ID J:15224)
  • premature death
    • onset of morbidity has a wide range, from 10 days to 10 weeks, with some surviving longer and to at least 19 weeks of age   (MGI Ref ID J:15224)
  • growth/size/body phenotype
  • abnormal snout morphology
    • rounded snout   (MGI Ref ID J:15224)
    • short snout   (MGI Ref ID J:15224)
  • decreased body size
    • decreased body size is first seen at 1 week of age and varies from mutant to mutant   (MGI Ref ID J:15224)
    • cachexia
      • mutants that become visibly ill are often lethargic, anorectic, wasted, and at times tremulous   (MGI Ref ID J:15224)
  • postnatal growth retardation
    • growth rate slows after puberty   (MGI Ref ID J:15224)
    • exhibit immature facial features at 1 week of age   (MGI Ref ID J:15224)
  • small ears   (MGI Ref ID J:15224)
  • hearing/vestibular/ear phenotype
  • small ears   (MGI Ref ID J:15224)
  • craniofacial phenotype
  • abnormal snout morphology
    • rounded snout   (MGI Ref ID J:15224)
    • short snout   (MGI Ref ID J:15224)
  • small ears   (MGI Ref ID J:15224)
  • immune system phenotype
  • abnormal CD4-positive T cell morphology
    • total numbers of CD4+ single positive thymocytes decrease over time   (MGI Ref ID J:15224)
  • abnormal CD8-positive T cell morphology
    • total numbers of CD8+ single positive thymocytes decrease over time   (MGI Ref ID J:15224)
  • abnormal immune system organ morphology
    • exhibit massive cell death in lymphoid organs as mice age, especially the spleen and thymus, resulting in lymphoid organ involution   (MGI Ref ID J:15224)
    • abnormal spleen morphology
      • spleen undergoes massive apoptotic involution with age   (MGI Ref ID J:15224)
      • abnormal spleen red pulp morphology
        • red pulp shows an increase in the proportion of erythroid relative to myeloid lineage cells   (MGI Ref ID J:15224)
      • abnormal spleen white pulp morphology
        • loss of white pulp lymphoid areas with age and illness; many pyknotic and fragmented cells are noted in white pulp   (MGI Ref ID J:15224)
      • small spleen
        • ill mutants exhibit a decrease in spleen size   (MGI Ref ID J:15224)
    • abnormal thymus morphology
      • exhibit widespread apoptosis in thymus as mutants age and become ill   (MGI Ref ID J:15224)
      • small thymus
        • ill mutants exhibit a decrease in thymus size, with increased apoptosis in both cortex and medulla   (MGI Ref ID J:15224)
  • abnormal thymus involution
    • exhibit involution of thymus with aging and illness   (MGI Ref ID J:15224)
  • decreased lymphocyte cell number
    • the percent of lymphocytes and absolute lymphocyte count are decreased in the peripheral blood of ill mutants (lymphopenia)   (MGI Ref ID J:15224)
    • decreased B cell number
      • exhibit a loss of peripheral B cells over time due to increased apoptosis   (MGI Ref ID J:15224)
    • decreased T cell number
      • exhibit a loss of peripheral T cells over time due to increased apoptosis   (MGI Ref ID J:15224)
      • decreased double-positive T cell number
        • loss of CD4+CD8+ double positive thymocytes over time   (MGI Ref ID J:15224)
  • increased T cell apoptosis
    • thymocytes show accelerated cell death following an apoptotic stimulates (dexamethasone and radiation) compared to wild-type   (MGI Ref ID J:15224)
  • increased double-negative T cell number
    • increase in double negative CD4-CD8- thymocytes over time   (MGI Ref ID J:15224)
  • renal/urinary system phenotype
  • abnormal kidney interstitium morphology
    • mice exhibit hyperproliferative interstitial components with increasing age   (MGI Ref ID J:15224)
    • kidneys have an abnormally abnundant interstitium that contains many cells with pyknotic nuclei within nests of immature appearing cells   (MGI Ref ID J:15224)
  • abnormal metanephric mesenchyme morphology
    • after 3 days in organ culture, tubulogenesis within the metanephric blastema is significantly reduced   (MGI Ref ID J:22552)
    • however, induction of the metanephric blastema occurs in vivo, with no significant differences in the size of metanephroi obtained from E12 mutant and control embryos   (MGI Ref ID J:22552)
    • increased metanephric mesenchyme apoptosis
      • abundant TUNEL-positive apoptotic cells in E12 metanephroi, esp. within the mesenchymal regions   (MGI Ref ID J:22552)
  • abnormal metanephric ureteric bud development
    • in organ culture, lack of nephrogenic development is confirmed by staining for lectin D. biflorus which stains the ureteric bud   (MGI Ref ID J:22552)
  • abnormal nephrogenic zone morphology
    • the size of nephrogenic zone is significantly reduced in neonatal kidneys   (MGI Ref ID J:22552)
  • abnormal renal glomerulus morphology
    • mice exhibit hyperproliferative glomerular epithelial components with increasing age   (MGI Ref ID J:15224)
    • decreased renal glomerulus number
      • fewer glomeruli are observed in neonatal kidneys relative to controls   (MGI Ref ID J:22552)
  • abnormal renal tubule epithelium morphology
    • mitotic figures, not usually found in mature kidneys, are seen in the hyperplastic tubular epithelium   (MGI Ref ID J:15224)
  • decreased nephron number
    • reduced nephron number at birth   (MGI Ref ID J:22552)
  • delayed kidney development
    • after P7, kidney growth, as reflected by increased size and weight, is significantly slowed relative to wild-type controls   (MGI Ref ID J:34504)
  • dilated distal convoluted tubules
    • distal tubular ectasia (dilation) is apparent by 1 week after birth   (MGI Ref ID J:15224)
  • dilated proximal convoluted tubules
    • proximal tubular ectasia (dilation) is apparent by 1 week after birth   (MGI Ref ID J:15224)
  • enlarged kidney
    • kidneys are either grossly enlarged and cystic or small and pale   (MGI Ref ID J:15224)
  • increased compensatory renal growth
    • by P21, unaffected glomeruli and non-cystic proximal tubules undergo compensatory growth   (MGI Ref ID J:34504)
  • increased kidney apoptosis
    • increased apoptosis of cells within cysts and in the renal interstitium at P28, as shown by TUNEL staining   (MGI Ref ID J:34504)
  • increased kidney cell proliferation
    • 87-fold increase in the number of BrdU-positive cells detected in the medulla at P28   (MGI Ref ID J:34504)
    • 1.9-fold increase in the number of BrdU-positive cells detected in the cortex at P28   (MGI Ref ID J:34504)
    • mice exhibit hyperproliferative glomerular epithelial and interstitial components with increasing age   (MGI Ref ID J:15224)
  • kidney cysts
    • grossly enlarged kidneys are cystic   (MGI Ref ID J:15224)
    • small kidneys show small cysts   (MGI Ref ID J:15224)
    • relatively few cysts at P7; however, marked cyst formation between P21 and p28   (MGI Ref ID J:34504)
    • at P21, cystic kidneys exhibit nuclear localization of beta-catenin and loss of apical brush border actin staining; however, protein levels of alpha-catenin, beta-catenin, actin, and E-cadherin are not altered in cystic kidneys relative to non-cystic kidneys   (MGI Ref ID J:53123)
    • kidney cortex cysts
      • detected at 1 week and 8 months of age   (MGI Ref ID J:22552)
      • cortex cysts of both proximal tubule and cortical collecting duct origin at P28   (MGI Ref ID J:34504)
    • kidney medulla cysts
      • cysts originating from the medullary thick ascending limb of Henle's loop and the medullary collecting ducts at P28   (MGI Ref ID J:34504)
    • polycystic kidney
      • develop polycystic kidney disease   (MGI Ref ID J:15224)
      • after P7, cysts develop at mutliple sites along the nephron   (MGI Ref ID J:34504)
  • kidney failure
    • severe renal insufficiency at 1-8 weeks of age, as shown by increased blood creatinine and BUN levels   (MGI Ref ID J:22552)
  • pale kidney
    • small kidneys are pale   (MGI Ref ID J:15224)
  • parietal capsular epithelium metaplasia
    • mice exhibit replacement of the normal flattened epithelium with a cuboidal proximal tubular epithelium and hyperplasia resulting in an immature epithelial crescent crowding the glomerulus, indicating tubular metaplasia of Bowman's epithelium   (MGI Ref ID J:15224)
  • small kidney
    • kidneys are either small and pale or grossly enlarged and cystic   (MGI Ref ID J:15224)
    • decreased kidney size at 1 week of age   (MGI Ref ID J:22552)
    • neonatal kidneys are not cystic but several-fold smaller than heterozygous control kidneys   (MGI Ref ID J:22552)
    • decreased kidney weight
      • approximately one-third of normal kidney weight at birth (P0)   (MGI Ref ID J:34504)
    • renal hypoplasia   (MGI Ref ID J:22552)
      • renal hypoplasia at P0   (MGI Ref ID J:34504)
  • small metanephros
    • after 3 days in organ culture, growth and development of E12 mutant metanephroi is visibly reduced   (MGI Ref ID J:22552)
  • homeostasis/metabolism phenotype
  • increased blood urea nitrogen level   (MGI Ref ID J:22552)
    • increases with age   (MGI Ref ID J:15224)
  • increased circulating creatinine level   (MGI Ref ID J:22552)
    • increases with age   (MGI Ref ID J:15224)
  • pigmentation phenotype
  • hypopigmentation
    • hair turns gray with the second follicle cycle   (MGI Ref ID J:15224)
    • hypopigmentation often begins at the nose and proceeds caudally over 3-4 days   (MGI Ref ID J:15224)
    • hair shafts still demonstrate the differentially pigmented regions seen in wild-type, however they are markedly lightened throughout   (MGI Ref ID J:15224)
    • Fontana-Mason stain shows the presence of melanin in all hairs, suggesting a decrease in dark pigment rather than a loss of melanocytes   (MGI Ref ID J:15224)
  • endocrine/exocrine gland phenotype
  • abnormal primordial ovarian follicle morphology
    • numerous aberrantly formed primordial follicles with a single layer of granulosa cells and lacking oocytes   (MGI Ref ID J:28173)
    • normal primary, preantral, and antral follicles, containing normal oocytes   (MGI Ref ID J:28173)
  • abnormal thymus involution
    • exhibit involution of thymus with aging and illness   (MGI Ref ID J:15224)
  • abnormal thymus morphology
    • exhibit widespread apoptosis in thymus as mutants age and become ill   (MGI Ref ID J:15224)
    • small thymus
      • ill mutants exhibit a decrease in thymus size, with increased apoptosis in both cortex and medulla   (MGI Ref ID J:15224)
  • reproductive system phenotype
  • abnormal primordial ovarian follicle morphology
    • numerous aberrantly formed primordial follicles with a single layer of granulosa cells and lacking oocytes   (MGI Ref ID J:28173)
    • normal primary, preantral, and antral follicles, containing normal oocytes   (MGI Ref ID J:28173)
  • absent oocytes
    • loss of oocytes in aberrant primordial follicles   (MGI Ref ID J:28173)
  • hematopoietic system phenotype
  • abnormal CD4-positive T cell morphology
    • total numbers of CD4+ single positive thymocytes decrease over time   (MGI Ref ID J:15224)
  • abnormal CD8-positive T cell morphology
    • total numbers of CD8+ single positive thymocytes decrease over time   (MGI Ref ID J:15224)
  • abnormal spleen morphology
    • spleen undergoes massive apoptotic involution with age   (MGI Ref ID J:15224)
    • abnormal spleen red pulp morphology
      • red pulp shows an increase in the proportion of erythroid relative to myeloid lineage cells   (MGI Ref ID J:15224)
    • abnormal spleen white pulp morphology
      • loss of white pulp lymphoid areas with age and illness; many pyknotic and fragmented cells are noted in white pulp   (MGI Ref ID J:15224)
    • small spleen
      • ill mutants exhibit a decrease in spleen size   (MGI Ref ID J:15224)
  • abnormal thymus involution
    • exhibit involution of thymus with aging and illness   (MGI Ref ID J:15224)
  • abnormal thymus morphology
    • exhibit widespread apoptosis in thymus as mutants age and become ill   (MGI Ref ID J:15224)
    • small thymus
      • ill mutants exhibit a decrease in thymus size, with increased apoptosis in both cortex and medulla   (MGI Ref ID J:15224)
  • decreased lymphocyte cell number
    • the percent of lymphocytes and absolute lymphocyte count are decreased in the peripheral blood of ill mutants (lymphopenia)   (MGI Ref ID J:15224)
    • decreased B cell number
      • exhibit a loss of peripheral B cells over time due to increased apoptosis   (MGI Ref ID J:15224)
    • decreased T cell number
      • exhibit a loss of peripheral T cells over time due to increased apoptosis   (MGI Ref ID J:15224)
      • decreased double-positive T cell number
        • loss of CD4+CD8+ double positive thymocytes over time   (MGI Ref ID J:15224)
  • increased T cell apoptosis
    • thymocytes show accelerated cell death following an apoptotic stimulates (dexamethasone and radiation) compared to wild-type   (MGI Ref ID J:15224)
  • increased double-negative T cell number
    • increase in double negative CD4-CD8- thymocytes over time   (MGI Ref ID J:15224)
  • cardiovascular system phenotype
  • abnormal pericyte morphology
    • exhibit a decreased number of pericytes in retinas   (MGI Ref ID J:96232)
  • abnormal retinal vasculature morphology
    • exhibit a significant decrease in retinal vascular density compared to wild-type; retinal vasculature contains less cellularity and fewer capillary loops   (MGI Ref ID J:96232)
    • exhibit delayed development and remodeling of retinal vasculature and a significant decrease in the number of major arteries, which branch off from near the optic nerve, however hyaloid vessel regression is not affected   (MGI Ref ID J:96232)
    • degree and extent of secondary and tertiary branching is compromised in retinal vasculature   (MGI Ref ID J:96232)
    • exhibit increased apoptosis and increased proliferation in the developing retinal vasculature   (MGI Ref ID J:96232)
    • abnormal induced retinal neovascularization
      • degree of ischemia-induced retinal neovascularization is reduced, however show a similar sensitivity to hyperoxia-mediated vessel obliteration   (MGI Ref ID J:96232)
  • decreased vascular endothelial cell number
    • exhibit a decreased number of endothelial cells in the retinas   (MGI Ref ID J:96232)
  • vision/eye phenotype
  • abnormal retinal vasculature morphology
    • exhibit a significant decrease in retinal vascular density compared to wild-type; retinal vasculature contains less cellularity and fewer capillary loops   (MGI Ref ID J:96232)
    • exhibit delayed development and remodeling of retinal vasculature and a significant decrease in the number of major arteries, which branch off from near the optic nerve, however hyaloid vessel regression is not affected   (MGI Ref ID J:96232)
    • degree and extent of secondary and tertiary branching is compromised in retinal vasculature   (MGI Ref ID J:96232)
    • exhibit increased apoptosis and increased proliferation in the developing retinal vasculature   (MGI Ref ID J:96232)
    • abnormal induced retinal neovascularization
      • degree of ischemia-induced retinal neovascularization is reduced, however show a similar sensitivity to hyperoxia-mediated vessel obliteration   (MGI Ref ID J:96232)
  • cellular phenotype
  • abnormal cell adhesion
    • at P21, cystic kidneys exhibit an altered distribution of beta-catenin and actin, suggesting that abnormal cell-cell adhesive interactions may contribute to cyst formation   (MGI Ref ID J:53123)
  • increased T cell apoptosis
    • thymocytes show accelerated cell death following an apoptotic stimulates (dexamethasone and radiation) compared to wild-type   (MGI Ref ID J:15224)
  • increased kidney apoptosis
    • increased apoptosis of cells within cysts and in the renal interstitium at P28, as shown by TUNEL staining   (MGI Ref ID J:34504)
  • increased kidney cell proliferation
    • 87-fold increase in the number of BrdU-positive cells detected in the medulla at P28   (MGI Ref ID J:34504)
    • 1.9-fold increase in the number of BrdU-positive cells detected in the cortex at P28   (MGI Ref ID J:34504)
    • mice exhibit hyperproliferative glomerular epithelial and interstitial components with increasing age   (MGI Ref ID J:15224)
  • increased metanephric mesenchyme apoptosis
    • abundant TUNEL-positive apoptotic cells in E12 metanephroi, esp. within the mesenchymal regions   (MGI Ref ID J:22552)

Bcl2tm1Sjk/Bcl2tm1Sjk

        B6;129S2-Bcl2tm1Sjk/J
  • muscle phenotype
  • abnormal skeletal muscle fiber type ratio
    • although soleus and tibialis anterior muscles show similar numbers of slow myofibers as in wild-type, the number of fast myofibers is only about 2/3 the number in wild-type   (MGI Ref ID J:66494)
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Research Applications
This mouse can be used to support research in many areas including:

Bcl2tm1Sjk related

Apoptosis Research
Endogenous Regulators

Cancer Research
Tumor Suppressor Genes

Developmental Biology Research
Growth Defects

Hematological Research
Hematopoietic Defects

Immunology, Inflammation and Autoimmunity Research
Immunodeficiency
Intracellular Signaling Molecules

Internal/Organ Research
Kidney Defects
      polycystic kidney disease
Spleen Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Bcl2tm1Sjk
Allele Name targeted mutation 1, Stanley J Korsmeyer
Allele Type Targeted (Null/Knockout)
Common Name(s) Bcl-2-; BclIItm1Sjk;
Mutation Made ByDr. Stanley Korsmeyer,   Dana-Farber Cancer Institute
Strain of Origin129S2/SvPas
ES Cell Line NameD3
ES Cell Line Strain129S2/SvPas
Gene Symbol and Name Bcl2, B cell leukemia/lymphoma 2
Chromosome 1
Gene Common Name(s) AW986256; Bcl-2; C430015F12Rik; D630044D05Rik; D830018M01Rik; PPP1R50; RIKEN cDNA C430015F12 gene; RIKEN cDNA D630044D05 gene; RIKEN cDNA D830018M01 gene; expressed sequence AW986256;
Molecular Note A 1.1 kb genomic fragment containing all of the coding region of exon 3 was replaced with a neomycin selection cassette. The authors state that no full length or truncated protein was detected in vitro or in vivo (data not shown). [MGI Ref ID J:15224]

Genotyping

Genotyping Information

Genotyping Protocols

Bcl2tm1Sjk, Standard PCR
Bcl2tm1Sjk, Standard PCR
NEOTD (Generic Neo), Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Veis DJ; Sorenson CM; Shutter JR; Korsmeyer SJ. 1993. Bcl-2-deficient mice demonstrate fulminant lymphoid apoptosis, polycystic kidneys, and hypopigmented hair. Cell 75(2):229-40. [PubMed: 8402909]  [MGI Ref ID J:15224]

Additional References

Adams JM; Cory S. 1998. The Bcl-2 protein family: arbiters of cell survival. Science 281(5381):1322-6. [PubMed: 9735050]  [MGI Ref ID J:49588]

Knudson CM; Korsmeyer SJ. 1997. Bcl-2 and Bax function independently to regulate cell death. Nat Genet 16(4):358-63. [PubMed: 9241272]  [MGI Ref ID J:42051]

Sorenson CM; Rogers SA; Korsmeyer SJ; Hammerman MR. 1995. Fulminant metanephric apoptosis and abnormal kidney development in bcl-2-deficient mice. Am J Physiol 268(1 Pt 2):F73-81. [PubMed: 7840250]  [MGI Ref ID J:22552]

Bcl2tm1Sjk related

Aarabi S; Bhatt KA; Shi Y; Paterno J; Chang EI; Loh SA; Holmes JW; Longaker MT; Yee H; Gurtner GC. 2007. Mechanical load initiates hypertrophic scar formation through decreased cellular apoptosis. FASEB J 21(12):3250-61. [PubMed: 17504973]  [MGI Ref ID J:143834]

Backman M; Machon O; Mygland L; van den Bout CJ; Zhong W; Taketo MM; Krauss S. 2005. Effects of canonical Wnt signaling on dorso-ventral specification of the mouse telencephalon. Dev Biol 279(1):155-68. [PubMed: 15708565]  [MGI Ref ID J:96233]

Chao DT; Linette GP; Boise LH; White LS; Thompson CB; Korsmeyer SJ. 1995. Bcl-XL and Bcl-2 repress a common pathway of cell death. J Exp Med 182(3):821-8. [PubMed: 7650488]  [MGI Ref ID J:78583]

Deckwerth TL; Easton RM; Knudson CM; Korsmeyer SJ; Johnson EM Jr. 1998. Placement of the BCL2 family member BAX in the death pathway of sympathetic neurons activated by trophic factor deprivation. Exp Neurol 152(1):150-62. [PubMed: 9682022]  [MGI Ref ID J:179272]

Dominov JA; Houlihan-Kawamoto CA; Swap CJ; Miller JB. 2001. Pro- and anti-apoptotic members of the bcl-2 family in skeletal muscle: A distinct role for bcl-2 in later stages of myogenesis Dev Dyn 220(1):18-26. [PubMed: 11146504]  [MGI Ref ID J:66494]

Gonzalez-Herrero I; Vicente-Duenas C; Orfao A; Flores T; Jimenez R; Cobaleda C; Sanchez-Garcia I. 2010. Bcl2 is not required for the development and maintenance of leukemia stem cells in mice. Carcinogenesis 31(7):1292-7. [PubMed: 20299524]  [MGI Ref ID J:161649]

Greenlund LJ; Korsmeyer SJ; Johnson EM Jr. 1995. Role of BCL-2 in the survival and function of developing and mature sympathetic neurons. Neuron 15(3):649-61. [PubMed: 7546744]  [MGI Ref ID J:119622]

Grutzmacher C; Park S; Elmergreen TL; Tang Y; Scheef EA; Sheibani N; Sorenson CM. 2010. Opposing effects of bim and bcl-2 on lung endothelial cell migration. Am J Physiol Lung Cell Mol Physiol 299(5):L607-20. [PubMed: 20656893]  [MGI Ref ID J:165746]

Hochman A; Liang H; Offen D; Melamed E; Sternin H. 2000. Developmental changes in antioxidant enzymes and oxidative damage in kidneys, liver and brain of bcl-2 knockout mice Cell Mol Biol (Noisy-Le-Grand) 46(1):41-52. [PubMed: 10726970]  [MGI Ref ID J:61247]

Hochman A; Sternin H; Gorodin S; Korsmeyer S; Ziv I; Melamed E; Offen D. 1998. Enhanced oxidative stress and altered antioxidants in brains of Bcl-2-deficient mice. J Neurochem 71(2):741-8. [PubMed: 9681465]  [MGI Ref ID J:111984]

Knudson CM; Korsmeyer SJ. 1997. Bcl-2 and Bax function independently to regulate cell death. Nat Genet 16(4):358-63. [PubMed: 9241272]  [MGI Ref ID J:42051]

Kondo S; Oakes MG; Sorenson CM. 2008. Rescue of renal hypoplasia and cystic dysplasia in Bcl-2 -/- mice expressing Bcl-2 in ureteric bud derived epithelia. Dev Dyn 237(9):2450-9. [PubMed: 18729219]  [MGI Ref ID J:138802]

Kondo S; Tang Y; Scheef EA; Sheibani N; Sorenson CM. 2008. Attenuation of retinal endothelial cell migration and capillary morphogenesis in the absence of bcl-2. Am J Physiol Cell Physiol 294(6):C1521-30. [PubMed: 18417716]  [MGI Ref ID J:136819]

Kurtulus S; Tripathi P; Moreno-Fernandez ME; Sholl A; Katz JD; Grimes HL; Hildeman DA. 2011. Bcl-2 allows effector and memory CD8+ T cells to tolerate higher expression of Bim. J Immunol 186(10):5729-37. [PubMed: 21451108]  [MGI Ref ID J:173111]

Linette GP; Li Y; Roth K; Korsmeyer SJ. 1996. Cross talk between cell death and cell cycle progression: BCL-2 regulates NFAT-mediated activation. Proc Natl Acad Sci U S A 93(18):9545-52. [PubMed: 8790367]  [MGI Ref ID J:153272]

Luciani DS; White SA; Widenmaier SB; Saran VV; Taghizadeh F; Hu X; Allard MF; Johnson JD. 2013. Bcl-2 and Bcl-xL suppress glucose signaling in pancreatic beta-cells. Diabetes 62(1):170-82. [PubMed: 22933114]  [MGI Ref ID J:208489]

Mason KD; Carpinelli MR; Fletcher JI; Collinge JE; Hilton AA; Ellis S; Kelly PN; Ekert PG; Metcalf D; Roberts AW; Huang DC; Kile BT. 2007. Programmed anuclear cell death delimits platelet life span. Cell 128(6):1173-86. [PubMed: 17382885]  [MGI Ref ID J:149205]

Middleton G; Cox SW; Korsmeyer S; Davies AM. 2000. Differences in bcl-2- and bax-independent function in regulating apoptosis in sensory neuron populations. Eur J Neurosci 12(3):819-27. [PubMed: 10762311]  [MGI Ref ID J:63350]

Nishimura EK; Granter SR; Fisher DE. 2005. Mechanisms of hair graying: incomplete melanocyte stem cell maintenance in the niche. Science 307(5710):720-4. [PubMed: 15618488]  [MGI Ref ID J:96016]

Ratts VS; Flaws JA; Kolp R; Sorenson CM; Tilly JL. 1995. Ablation of bcl-2 gene expression decreases the numbers of oocytes and primordial follicles established in the post-natal female mouse gonad. Endocrinology 136(8):3665-8. [PubMed: 7628407]  [MGI Ref ID J:28173]

Snow JW; Abraham N; Ma MC; Bronson SK; Goldsmith MA. 2003. Transgenic bcl-2 is not sufficient to rescue all hematolymphoid defects in STAT5A/5B-deficient mice. Exp Hematol 31(12):1253-8. [PubMed: 14662332]  [MGI Ref ID J:115667]

Sorenson CM. 1999. Nuclear localization of beta-catenin and loss of apical brush border actin in cystic tubules of bcl-2 -/- mice. Am J Physiol 276(2 Pt 2):F210-7. [PubMed: 9950951]  [MGI Ref ID J:53123]

Sorenson CM; Padanilam BJ; Hammerman MR. 1996. Abnormal postpartum renal development and cystogenesis in the bcl-2 (-/-) mouse. Am J Physiol 271(1 Pt 2):F184-93. [PubMed: 8760259]  [MGI Ref ID J:34504]

Sorenson CM; Rogers SA; Korsmeyer SJ; Hammerman MR. 1995. Fulminant metanephric apoptosis and abnormal kidney development in bcl-2-deficient mice. Am J Physiol 268(1 Pt 2):F73-81. [PubMed: 7840250]  [MGI Ref ID J:22552]

Thompson J; Winoto A. 2008. During negative selection, Nur77 family proteins translocate to mitochondria where they associate with Bcl-2 and expose its proapoptotic BH3 domain. J Exp Med 205(5):1029-36. [PubMed: 18443228]  [MGI Ref ID J:136238]

Tikhonova AN; Van Laethem F; Hanada K; Lu J; Pobezinsky LA; Hong C; Guinter TI; Jeurling SK; Bernhardt G; Park JH; Yang JC; Sun PD; Singer A. 2012. alphabeta T Cell Receptors that Do Not Undergo Major Histocompatibility Complex-Specific Thymic Selection Possess Antibody-like Recognition Specificities. Immunity 36(1):79-91. [PubMed: 22209676]  [MGI Ref ID J:180750]

Wang S; Sorenson CM; Sheibani N. 2005. Attenuation of retinal vascular development and neovascularization during oxygen-induced ischemic retinopathy in Bcl-2-/- mice. Dev Biol 279(1):205-19. [PubMed: 15708569]  [MGI Ref ID J:96232]

Wojciechowski S; Tripathi P; Bourdeau T; Acero L; Grimes HL; Katz JD; Finkelman FD; Hildeman DA. 2007. Bim/Bcl-2 balance is critical for maintaining naive and memory T cell homeostasis. J Exp Med 204(7):1665-75. [PubMed: 17591857]  [MGI Ref ID J:125868]

Yamashita J; Datta NS; Chun YH; Yang DY; Carey AA; Kreider JM; Goldstein SA; McCauley LK. 2008. Role of Bcl2 in osteoclastogenesis and PTH anabolic actions in bone. J Bone Miner Res 23(5):621-32. [PubMed: 18086008]  [MGI Ref ID J:150177]

Zhang N; He YW. 2005. The antiapoptotic protein Bcl-xL is dispensable for the development of effector and memory T lymphocytes. J Immunol 174(11):6967-73. [PubMed: 15905539]  [MGI Ref ID J:99012]

Ziehr J; Sheibani N; Sorenson CM. 2004. Alterations in cell-adhesive and migratory properties of proximal tubule and collecting duct cells from bcl-2 -/- mice. Am J Physiol Renal Physiol 287(6):F1154-63. [PubMed: 15292044]  [MGI Ref ID J:95643]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2140.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We willfulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2782.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We willfulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Control Information

  Control
   Wild-type from the colony
   101045 B6129SF2/J (approximate)
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.


See Terms of Use tab for General Terms and Conditions


The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.

Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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