JAX Mouse Strain Datasheet - 008238

129S-Sele^tm1Dmil/J

Stock No:: 008238

Cryo Recovery

Overview

Also Known As: 129SvEv congenic E-selectin

These E-selectin mutant mice may be useful in studying inflammation, leukocyte rolling, leukocyte-endothelial adhesion, angiogenesis, and cancer.

Donating Investigator

David S Milstone, Brigham and Women's Hospital

Genetic overview

Genetic Background	Generation

Sele^tm1Dmil

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Sele	selectin, endothelial cell

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Research Applications

Cancer Research
Cardiovascular Research
Cell Biology Research
Developmental Biology Research
Immunology, Inflammation and Autoimmunity Research
Internal/Organ Research
Research Tools

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Base Price

Starting at:

$2,595.00 Domestic price Cryo Recovery

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Details

Detailed Description

Mice homozygous for this E-selectin mutant allele (E^-/-) are viable and fertile with normal circulating leukocyte and platelet profiles. While several transcripts are generated from the mutant locus (due to transcription from the endogenous promoter and/or bidirectional transcription initiated from the pgk promoter in the neo-resistance cassette), these frame-shifted transcripts are non-functional with several predicted stop codons. In contrast to wildtype mice, no protein product is detected in several tissues isolated from LPS-injected homozygous mice. Homozygous mice exhibit abnormal responses to inflammatory stimuli. E-selectin deficiency results in endostatin unresponsiveness (as shown in corneal angiogenesis (mixed B6;129 genetic background) and aortic explant (C57BL/6 congenic background) experiments). These E-selectin mutant mice may be useful in studying inflammation, leukocyte rolling, leukocyte-endothelial adhesion, angiogenesis, and cancer.

Of note, E-selectin mutant mice are also be available on a C57BL/6J congenic background (Stock No. 008236), a BALB/cJ congenic background (Stock No. 008237), on a mixed genetic background (Stock No. 002915), and along with other selectin mutations (Stock No. 002916, Stock No. 003806, and Stock No. 003807).

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype of these E-selectin mutant mice could vary from that originally described. We will modify the strain description if necessary as published results become available.

Development

A targeting vector was designed to replace exons 1-3 of the targeted gene with a reverse-oriented PGK-neo cassette. The construct was electroporated into 129S4/SvJae-derived J1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into blastocysts and chimeric males were bred with C57BL/6J to generate mutant mice. Next, mutant mice were backcrossed to 129S6/SvEvTac inbred mice for 11 generations prior to arrival at The Jackson Laboratory. The Y chromosome may not have been fixed to the genetic background during the backcross.

Control Suggestions

Approximate Controls

None Available

Additional Information

Considerations for Choosing Controls

Selected References

Milstone DS; Fukumura D; Padgett RC; O'Donnell PE; Davis VM; Benavidez OJ; Monsky WL; Melder RJ; Jain RK; Gimbrone MA Jr. 1998. Mice lacking E-selectin show normal numbers of rolling leukocytes but reduced leukocyte stable arrest on cytokine-activated microvascular endothelium. Microcirculation 5(2-3):153-71. PubMed: 9789256 MGI: J:113169

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Genetics

Sele^tm1Dmil

Allele Symbol: Sele^tm1Dmil

Allele Name	targeted mutation 1, David Milstone
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	E-selectin^-; E^-
Gene Symbol and Name	Sele, selectin, endothelial cell
Gene Synonym(s)	CD62E; E-selectin; ELAM; ELAM1; ESEL; Elam; Elam; LECAM2; endothelial adhesion molecule
Strain of Origin	129S4/SvJae
Chromosome	1
Molecular Note	The neomycin resistance gene was substituted in reverse transcriptional orientation for sequence spanning from exon 1 to exon 3. Northern blot confirmed absence of transcript in mutant kidney, lung and heart samples.
Mutations Made By	David Milstone, Brigham and Women's Hospital

Disease/Phenotype

Disease Terms

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Cancer Research
- Defects in Cell Adhesion Molecules
Cardiovascular Research
- Vascular Defects
  - defective leukocyte function
Cell Biology Research
- Defects in Cell Adhesion Molecules
Developmental Biology Research
- Defects in Cell Adhesion Molecules
Immunology, Inflammation and Autoimmunity Research
- Inflammation
- Lymphoid Tissue Defects
Internal/Organ Research
- Lymphoid Tissue Defects
Research Tools
- Cancer Research
- Cardiovascular Research
- Cell Biology Research
- Immunology, Inflammation and Autoimmunity Research

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Sele^tm1Dmil/Sele^tm1Dmil
involves: 129S4/SvJae * C57BL/6J

immune system phenotype

abnormal leukocyte adhesion
- TNFa treatment to stimulate an inflammatory response resulted in a significantly lower amount of adhesion in mutants vs wild-type
- in mutants, fewer dermal microvessels support high adhesion densities compared to wild-type mice; a similar trend is observed in mesenteric microvessels
- numbers of adherent cells in wild-type prior to treatment is 74 adherent cells/sq. mm and in mutants 83 cells/sq. mm.; after TNF treatment, in wild-type there are 1745 adherent cells/sq. mm while in mutants there are 798 cells/sq. mm

cellular phenotype

abnormal leukocyte adhesion
- TNFa treatment to stimulate an inflammatory response resulted in a significantly lower amount of adhesion in mutants vs wild-type
- in mutants, fewer dermal microvessels support high adhesion densities compared to wild-type mice; a similar trend is observed in mesenteric microvessels
- numbers of adherent cells in wild-type prior to treatment is 74 adherent cells/sq. mm and in mutants 83 cells/sq. mm.; after TNF treatment, in wild-type there are 1745 adherent cells/sq. mm while in mutants there are 798 cells/sq. mm

hematopoietic system phenotype

abnormal leukocyte adhesion
- TNFa treatment to stimulate an inflammatory response resulted in a significantly lower amount of adhesion in mutants vs wild-type
- in mutants, fewer dermal microvessels support high adhesion densities compared to wild-type mice; a similar trend is observed in mesenteric microvessels
- numbers of adherent cells in wild-type prior to treatment is 74 adherent cells/sq. mm and in mutants 83 cells/sq. mm.; after TNF treatment, in wild-type there are 1745 adherent cells/sq. mm while in mutants there are 798 cells/sq. mm

References

Milstone DS; Fukumura D; Padgett RC; O'Donnell PE; Davis VM; Benavidez OJ; Monsky WL; Melder RJ; Jain RK; Gimbrone MA Jr. 1998. Mice lacking E-selectin show normal numbers of rolling leukocytes but reduced leukocyte stable arrest on cytokine-activated microvascular endothelium. Microcirculation 5(2-3):153-71. PubMed: 9789256 MGI: J:113169

Additional - Sele^tm1Dmil related

Bae SJ; Shimizu K; Yozaki M; Yamaoka T; Akiyama Y; Yoshizaki A; Muroi E; Hara T; Ogawa F; Sato S. 2010. Involvement of L-selectin in contact hypersensitivity responses augmented by auditory stress. Am J Pathol 176(1):187-97. PubMed: 19948832 MGI: J:156378
Gerritsen ME; Shen CP; Atkinson WJ; Padgett RC; Gimbrone MA Jr; Milstone DS. 1996. Microvascular endothelial cells from E-selectin-deficient mice form tubes in vitro. Lab Invest 75(2):175-84. PubMed: 8765318 MGI: J:34956
Hiratsuka S; Goel S; Kamoun WS; Maru Y; Fukumura D; Duda DG; Jain RK. 2011. Endothelial focal adhesion kinase mediates cancer cell homing to discrete regions of the lungs via E-selectin up-regulation. Proc Natl Acad Sci U S A 108(9):3725-30. PubMed: 21321210 MGI: J:170481
Lebensburger JD; Howard T; Hu Y; Pestina TI; Gao G; Johnson M; Zakharenko SS; Ware RE; Tuomanen EI; Persons DA; Rosch JW. 2012. Hydroxyurea therapy of a murine model of sickle cell anemia inhibits the progression of pneumococcal disease by down-modulating E-selectin. Blood 119(8):1915-21. PubMed: 22130804 MGI: J:181749
Milstone DS; Redline RW; O'Donnell PE; Davis VM; Stavrakis G. 2000. E-selectin expression and function in a unique placental trophoblast population at the fetal-maternal interface: regulation by a trophoblast-restricted transcriptional mechanism conserved between humans and mice. Dev Dyn 219(1):63-76. PubMed: 10974672 MGI: J:64541
Yu Y; Moulton KS; Khan MK; Vineberg S; Boye E; Davis VM; O'Donnell PE; Bischoff J; Milstone DS. 2004. E-selectin is required for the antiangiogenic activity of endostatin. Proc Natl Acad Sci U S A 101(21):8005-10. PubMed: 15148373 MGI: J:90657

Pricing & Availability

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Genotype

Price

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Cryorecovery - Pricing

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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 will fulfill 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.

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.

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Also Known As: 129SvEv congenic E-selectin

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Approximate Controls

Additional Information

Selected References

Seletm1Dmil

Allele Symbol: Seletm1Dmil

Disease Terms

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Mammalian Phenotype Terms by Genotype

Genotype: Seletm1Dmil/Seletm1Dmilinvolves: 129S4/SvJae * C57BL/6J

immune system phenotype

cellular phenotype

hematopoietic system phenotype

References

Additional - Seletm1Dmil related

Genotyping Protocols

Breeding Considerations

Animal Health Reports

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

Live Mouse

Cryorecovery - Pricing

Progeny testing is not required

RELATED PRODUCTS AND SERVICES

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms of Use

Additional Use Restrictions Apply

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Sele^tm1Dmil

Allele Symbol: Sele^tm1Dmil

Genotype: Sele^tm1Dmil/Sele^tm1Dmil
involves: 129S4/SvJae * C57BL/6J

Additional - Sele^tm1Dmil related