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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID 		Cd38tm1Lnd
targeted mutation 1, Frances E Lund
MGI:1861803
Summary 4 genotypes


Genotype
MGI:3723582
hm1
Allelic
Composition		 Cd38tm1Lnd/Cd38tm1Lnd
Genetic
Background		 B6.129P2-Cd38tm1Lnd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd38tm1Lnd mutation (4 available); any Cd38 mutation (50 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
endocrine/exocrine glands
increased pancreatic islet cell apoptosis ( J:116576 )
• islets are significantly more susceptible to apoptosis at physiological glucose concentrations, in the presences of palmitate, or in the absence of serum
decreased pancreatic beta cell mass ( J:116576 )
• small but significant decrease in beta cell mass is observed under normal diet and high-fat feeding relative to controls
disorganized pancreatic islets ( J:116576 )
• disrupted islet architecture is observed
• glucagon-containing alpha cells are distributed diffusely between beta cells, whereas in wild-type islets, alpha cells are exclusively in the islet mantle

homeostasis/metabolism
homeostasis/metabolism phenotype ( J:116576 )
N
• blood glucose is not significantly different from wild-type regardless of diet
• glucose tolerance does not differ significantly, but there is a trend toward higher 30-minute glucose values in female mutants on both normal and high-fat diets
• insulin tolerance is similar to wild-type on both normal and high-fat diets
insulin resistance ( J:116576 )
• significant insulin resistance is observed in mice fed a high-fat diet

cellular
increased pancreatic islet cell apoptosis ( J:116576 )
• islets are significantly more susceptible to apoptosis at physiological glucose concentrations, in the presences of palmitate, or in the absence of serum




Genotype
MGI:2662016
hm2
Allelic
Composition		 Cd38tm1Lnd/Cd38tm1Lnd
Genetic
Background		 involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd38tm1Lnd mutation (4 available); any Cd38 mutation (50 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
immune system
abnormal humoral immune response ( J:49170 )
• in response to immunization with the TD antigen TNP(5)-KLH in alum adjuvant, mutants exhibit decreased hapten-specific IgM, IgG1, and IgE responses but mount normal hapten-specific IgG2a, IgG2b, IgG3 and IgA responses, however when mutants are immunized with TNP(5)-KLH in Freund's adjuvant, primary antibody responses are not different from wild-type
• mutants fail to mount significant secondary hapten-specific antibody responses
• mutants show elevated antibody responses to the TI-2 antigen alpha1-3 dextran but not to NP(27)-Ficoll

homeostasis/metabolism
abnormal enzyme/coenzyme activity ( J:49170 )
• NAD+ glycohydrolase activity in the spleen is reduced to less than 1% of the activity seen in wild-type spleens and no activity is detected in the liver and brain




Genotype
MGI:3623958
hm3
Allelic
Composition		 Cd38tm1Lnd/Cd38tm1Lnd
Genetic
Background		 NOD.129P2(B6)-Cd38tm1Lnd/LtJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd38tm1Lnd mutation (4 available); any Cd38 mutation (50 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
immune system
increased T cell apoptosis ( J:108097 )
• Cd38-deficient NOD mice display higher NAD-mediated T cell death
insulitis ( J:108097 )
• insulitis progression in null NOD mice is accelerated at 9 weeks or later compared to wild-type NOD mice
increased susceptibility to autoimmune diabetes ( J:108097 )
• homozygous NOD mutants show significant acceleration in diabetes development compared to wild-type NOD mice; the first diagnosis of diabetes is made at 10 weeks of age while in wild-type NOD mice it occurs at 12 weeks or later; the frequency in null NOD males is 100% by 28 weeks which is higher than the frequency in wild-type NOD males
• diabetes acceleration is seen only when Cd38-deficient bone marrow from NOD mice is transferred to Cd38-deficient recipients
• diabetes onset is assessed by 2 consecutive positive urine glucose tests

endocrine/exocrine glands
insulitis ( J:108097 )
• insulitis progression in null NOD mice is accelerated at 9 weeks or later compared to wild-type NOD mice

cellular
increased T cell apoptosis ( J:108097 )
• Cd38-deficient NOD mice display higher NAD-mediated T cell death

hematopoietic system
increased T cell apoptosis ( J:108097 )
• Cd38-deficient NOD mice display higher NAD-mediated T cell death

Mouse Models of Human Disease
 DO ID OMIM ID(s) Ref(s)
type 1 diabetes mellitus DOID:9744 OMIM:222100
 J:108097




Genotype
MGI:3623961
cx4
Allelic
Composition		 Art2atm1Fkn/Art2atm1Fkn
Art2btm1Fkn/Art2btm1Fkn
Cd38tm1Lnd/Cd38tm1Lnd
Genetic
Background		 NOD.129(B6)-Cd38tm1Lnd Art2atm1Fkn Art2btm1Fkn/Lt
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Art2atm1Fkn mutation (2 available); any Art2a mutation (9 available)
Art2btm1Fkn mutation (3 available); any Art2b mutation (23 available)
Cd38tm1Lnd mutation (4 available); any Cd38 mutation (50 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
immune system
decreased susceptibility to autoimmune diabetes ( J:108097 )
• double knockout NOD mice exhibit strong protection from diabetes in both sexes; female knockouts acquire diabetes at a frequency of 25% by 28 weeks compared to 100% in Cd38-null NOD females; double knockout NOD males are completely protected at 28 weeks compared to 100% incidence in Cd38-null NOD males




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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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Send questions and comments to User Support. 		last database update
04/23/2024
MGI 6.23 		The Jackson Laboratory