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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Ern1tm1Rjk
targeted mutation 1, Randal J Kaufman
MGI:3622330
Summary 3 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Ern1tm1Rjk/Ern1tm1Rjk involves: 129S1/Sv * 129X1/SvJ MGI:3723591
hm2
Ern1tm1Rjk/Ern1tm1Rjk involves: 129S1/Sv * 129X1/SvJ * C57BL/6J MGI:3625033
cn3
Ern1tm1Rjk/Ern1tm2.1Rjk
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA MGI:4949418


Genotype
MGI:3723591
hm1
Allelic
Composition
Ern1tm1Rjk/Ern1tm1Rjk
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ern1tm1Rjk mutation (0 available); any Ern1 mutation (57 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• expression of one unfolded protein response target genes, Edem, is decreased in mouse embryonic fibroblasts stressed with tunicamycin or thapsigargin results




Genotype
MGI:3625033
hm2
Allelic
Composition
Ern1tm1Rjk/Ern1tm1Rjk
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ern1tm1Rjk mutation (0 available); any Ern1 mutation (57 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• homozygous embryos die around E10.5
• Background Sensitivity: by backcrossing these heterozygotes further onto C57BL/6J, homozygous embryos which survive to E12.5-13 are produced

embryo
• at E13 homozygotes exhibit growth retardation
• by E13 homozygotes can be recognized by their small size

growth/size/body
• at E13 homozygotes exhibit growth retardation
• by E13 homozygotes can be recognized by their small size

hematopoietic system
• hematopoietic cells from null mice have a 2.5-fold lower rate of proliferation than the rate of heterozygous cell proliferation
• Ern1-null pro-B cells are defective in VDJ recombination of immunoglobulin genes and do not express B cell receptors

immune system
• Ern1-null pro-B cells are defective in VDJ recombination of immunoglobulin genes and do not express B cell receptors

liver/biliary system
• at E12.5, homozygous fetal livers are markedly reduced in size compared to wild-type

integument




Genotype
MGI:4949418
cn3
Allelic
Composition
Ern1tm1Rjk/Ern1tm2.1Rjk
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ern1tm1Rjk mutation (0 available); any Ern1 mutation (57 available)
Ern1tm2.1Rjk mutation (0 available); any Ern1 mutation (57 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (6 available); any Speer6-ps1 mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• 5-times in response to Bortezomib treatment
• following tamoxifen treatment
• following partial hepatectomy
• in response to Bortezomib treatment
• liver cells exhibit less rough endoplasmic reticulum content compared with control liver cells
• mice exhibit a slight increase in hepatic lipid content compared with control mice
• mice subjected to liver stress (partial hepatectomy or treatment with tamoxifen or Bortezomib) exhibit increased accumulation of lipids in the liver compared with control mice
• however, phospholipid synthesis is normal

homeostasis/metabolism
• mice exhibit a slight increase in hepatic lipid content compared with control mice
• mice subjected to liver stress (partial hepatectomy or treatment with tamoxifen or Bortezomib) exhibit increased accumulation of lipids in the liver compared with control mice
• however, phospholipid levels in the liver are normal
• following tamoxifen-treatment
• following tamoxifen treatment
• following partial hepatectomy
• in response to Bortezomib treatment
• following tamoxifen-treatment, secretion of apolipoproteins from liver cells is decreased compared to in control mice

cellular
• 5-times in response to Bortezomib treatment





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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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last database update
04/23/2024
MGI 6.23
The Jackson Laboratory