All Phenotypes Casp1<tm1Sesh> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
cx1	Casp1^tm1Sesh/Casp1^tm1Sesh Casp4^del/Casp4^del	B10.Cg-Casp1^tm1Sesh Casp4^del H2^r H2-T18^b	MGI:3581549
cx2	Casp1^tm1Sesh/Casp1^tm1Sesh Casp4^del/Casp4^del Slc11a1^s/Slc11a1^s	B6.129S2-Casp1^tm1Sesh Casp4^del	MGI:3851239
cx3	Casp1^tm1Sesh/Casp1^tm1Sesh Casp4^del/Casp4^del	B6.129S2(NOD)-Casp1^tm1Sesh Casp4^del	MGI:5468971
cx4	Casp1^tm1Sesh/Casp1^tm1Sesh Casp4^del/Casp4^del	C3.129S2-Casp1^tm1Sesh Casp4^del	MGI:4839936
cx5	Casp1^tm1Sesh/Casp1^tm1Sesh Casp4^del/Casp4^del	C3N.129S2-Casp1^tm1Sesh Casp4^del	MGI:3581548
cx6	Casp1^tm1Sesh/Casp1^tm1Sesh Casp4^del/Casp4^del	involves: 129 * 129S2/SvPas * C57BL/6	MGI:4360918
cx7	Casp1^tm1Sesh/Casp1⁺ Casp4^del/Casp4⁺	involves: 129S1/SvImJ * 129S2/SvPas * NOD	MGI:3696112
cx8	Casp1^tm1Sesh/Casp1^tm1Sesh Nlrp1a^Neut1/Nlrp1a^Neut1	involves: 129S2/SvPas * C57BL/6	MGI:5474285
cx9	Casp1^tm1Sesh/Casp1⁺ Casp4^del/Casp4⁺	involves: 129S2/SvPas * C57BL/6	MGI:3574069
cx10	Casp1^tm1Sesh/Casp1^tm1Sesh Casp4^del/Casp4^del	involves: 129S2/SvPas * C57BL/6	MGI:3574053
cx11	Casp1^tm1Sesh/Casp1^tm1Sesh Casp4^del/Casp4^del Tg(Casp4)#Gne/0	involves: 129S2/SvPas * C57BL/6 * NOD/ShiLtJ	MGI:5468972
cx12	Casp1^tm1Sesh/Casp1^tm1Sesh Casp4^del/Casp4^del Slc11a1^r/Slc11a1^s	involves: 129/Sv * 129S2/SvPas * C57BL/6	MGI:3851240
cx13	Casp1^tm1Sesh/Casp1^tm1Sesh Casp4^del/Casp4^del	NOD.129S2(B6)-Casp1^tm1Sesh Casp4^del/LtJ	MGI:3581521

Allelic Composition	Casp1^tm1Sesh/Casp1^tm1Sesh Casp4^del/Casp4^del
Genetic Background	B10.Cg-Casp1^tm1Sesh Casp4^del H2^r H2-T18^b

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

decreased susceptibility to bacterial infection induced morbidity/mortality ( J:63488 )

• homozygotes exhibit increased resistance to Salmonella infection with an oral S. typhimurium 50% lethal dose (LD50) that is 1,000-fold higher than that of wild-type mice

• following oral infection with an oral dose of S. typhimurium that is 100-fold higher than the LD50 in homozygotes, death occurs about 4 days later relative to wild-type mice

immune system

decreased inflammatory response ( J:63488 )

• following oral infection, Salmonella breachs the M cell barrier of mutant mice efficiently; however, homozygotes show a significant reduction in the number of intracellular bacteria and the recruitment of polymorphonuclear lymphocytes in Peyer's patches relative to wild-type mice

• in vitro, mutant macrophages are not inherently different in their capacity to kill Salmonella relative to wild-type-derived macrophages

decreased susceptibility to bacterial infection ( J:63488 )

• following oral infection, Salmonella fails disseminate systemically with significantly reduced colonization in the Peyer's patches, mesenteric lymph nodes, and spleens after an oral dose of S. typhimurium that is 100-fold higher than the LD50; in homozygotes, death occurs about 4 days later relative to wild-type mice

• notably, homozygotes and wild-type mice are equally susceptible to intraperitoneally injected Salmonella (100 SL1344 bacteria), exhibiting comparable spleen colonization and mortality

• in addition, homozygotes and wild-type are equally susceptible to colonization by Yersinia pseudotuberculosis, another enteric pathogen that normally invades the Peyer's patches

decreased susceptibility to bacterial infection induced morbidity/mortality ( J:63488 )

• homozygotes exhibit increased resistance to Salmonella infection with an oral S. typhimurium 50% lethal dose (LD50) that is 1,000-fold higher than that of wild-type mice

• following oral infection with an oral dose of S. typhimurium that is 100-fold higher than the LD50 in homozygotes, death occurs about 4 days later relative to wild-type mice

cellular

decreased apoptosis ( J:63488 )

• after an oral dose of S. typhimurium that is 100-fold higher than the LD50, homozygotes show significantly less apoptotic cells in Peyer's patches (PP); in contrast, increased apoptosis in wild-type PP correlates with colonization

Allelic Composition	Casp1^tm1Sesh/Casp1^tm1Sesh Casp4^del/Casp4^del Slc11a1^s/Slc11a1^s
Genetic Background	B6.129S2-Casp1^tm1Sesh Casp4^del

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Casp1^tm1Sesh mutation (5 available); any Casp1 mutation (42 available)
Casp4^del mutation (5 available); any Casp4 mutation (33 available)
Slc11a1^s mutation (0 available); any Slc11a1 mutation (40 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

immune system

abnormal macrophage physiology ( J:112400 )

• macrophages are resistant to cytotoxicity induced by in vitro Salmonella infection

increased susceptibility to bacterial infection ( J:112400 )

• mice succumb more rapidly than controls to 10⁸ CFU of Salmonella with a median survival time of 6 days compared to 8 days for controls

• there is an average 30-fold-higher bacterial loads in infected Peyer's patches, mesenteric lymph nodes, and spleens than in the infected organs of wild-type animals

hematopoietic system

abnormal macrophage physiology ( J:112400 )

• macrophages are resistant to cytotoxicity induced by in vitro Salmonella infection

Allelic Composition	Casp1^tm1Sesh/Casp1^tm1Sesh Casp4^del/Casp4^del
Genetic Background	B6.129S2(NOD)-Casp1^tm1Sesh Casp4^del

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

decreased susceptibility to xenobiotic induced morbidity/mortality ( J:193522 )

• in response to LPS challenge in a model of acute septic shock

immune system

decreased macrophage apoptosis ( J:193522 )

• impaired cell death in response to ATP, Clostridium difficile toxin B, CTB and E. coli

decreased circulating interleukin-1 alpha level ( J:193522 )

• in response to LPS challenge in a model of acute septic shock

decreased circulating interleukin-1 beta level ( J:193522 )

• in response to LPS challenge in a model of acute septic shock

decreased circulating interleukin-18 level ( J:193522 )

• in response to LPS challenge in a model of acute septic shock

decreased interleukin-1 alpha secretion ( J:193522 )

• from LPS-primed bone marrow-derived macrophage in response to ATP, C. difficile, CTB and E. coli

decreased interleukin-1 beta secretion ( J:193522 )

• LPS-primed bone marrow-derived macrophages fail to produce IL1b and IL18 in response to ATP, Clostridium difficile toxin B, cholera toxin B (CTB) or E. coli unlike controls

decreased interleukin-18 secretion ( J:193522 )

• LPS-primed bone marrow-derived macrophages fail to produce IL1b and IL18 in response to ATP, Clostridium difficile toxin B, cholera toxin B (CTB) or E. coli unlike controls

decreased susceptibility to endotoxin shock ( J:193522 )

• mice are resistant to LPS challenge in a model of acute septic shock with reduced mortality and serum levels of IL1b, IL1a and IL18

cellular

decreased apoptosis ( J:243487 )

• of intestinal epithelial cells (IECs) after oral rotavirus inoculation of 8 day old pups

decreased macrophage apoptosis ( J:193522 )

• impaired cell death in response to ATP, Clostridium difficile toxin B, CTB and E. coli

homeostasis/metabolism

decreased circulating interleukin-1 alpha level ( J:193522 )

• in response to LPS challenge in a model of acute septic shock

decreased circulating interleukin-1 beta level ( J:193522 )

• in response to LPS challenge in a model of acute septic shock

decreased circulating interleukin-18 level ( J:193522 )

• in response to LPS challenge in a model of acute septic shock

decreased susceptibility to xenobiotic induced morbidity/mortality ( J:193522 )

• in response to LPS challenge in a model of acute septic shock

hematopoietic system

decreased macrophage apoptosis ( J:193522 )

• impaired cell death in response to ATP, Clostridium difficile toxin B, CTB and E. coli

Allelic Composition	Casp1^tm1Sesh/Casp1^tm1Sesh Casp4^del/Casp4^del
Genetic Background	C3.129S2-Casp1^tm1Sesh Casp4^del

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

increased susceptibility to bacterial infection induced morbidity/mortality ( J:136368 )

• following infection with Sterne 34F2 strain of Bacillus anthracis

immune system

abnormal macrophage physiology ( J:136368 )

• macrophages exhibit impaired ability to kill Bacillus anthracis compared with wild-type cells

decreased interleukin-1 beta secretion ( J:136368 )

• following exposure of macrophages to LPS or Bacillus anthracis spores

increased susceptibility to bacterial infection ( J:136368 )

• following infection with Sterne 34F2 strain of Bacillus anthracis, mice exhibit increased mortality and reduced clearing compared with similarly treated wild-type mice

increased susceptibility to bacterial infection induced morbidity/mortality ( J:136368 )

• following infection with Sterne 34F2 strain of Bacillus anthracis

hematopoietic system

abnormal macrophage physiology ( J:136368 )

• macrophages exhibit impaired ability to kill Bacillus anthracis compared with wild-type cells

Allelic Composition	Casp1^tm1Sesh/Casp1^tm1Sesh Casp4^del/Casp4^del
Genetic Background	C3N.129S2-Casp1^tm1Sesh Casp4^del

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

immune system

abnormal response to infection ( J:86761 )

• following inoculation with neurovirulent ts-1 MuLV, both homozygotes and their respective control heterozygote littermates develop hind limb paralysis with comparable latencies and spongiform lesions of comparable severity

• lack of protection from MuLV-induced neurodegeneration suggests that pathways of neuronal cell death induced by ts-1 MuLV and hypoxia or ischemia are not identical

Allelic Composition	Casp1^tm1Sesh/Casp1^tm1Sesh Casp4^del/Casp4^del
Genetic Background	involves: 129 * 129S2/SvPas * C57BL/6

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

immune system

decreased interleukin-1 beta secretion ( J:50775 )

• freshly isolated peritoneal exudate cells (neutrophils and B cells) secrete less IL-1beta in response to LPS than in controls

• IL-1beta response to soluble FasL is similar to controls

Allelic Composition	Casp1^tm1Sesh/Casp1⁺ Casp4^del/Casp4⁺
Genetic Background	involves: 129S1/SvImJ * 129S2/SvPas * NOD

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

immune system

abnormal macrophage physiology ( J:99748 )

• Casp1-deficient bone marrow-derived macrophages that are homozygous for the 129S1 Nlrp1b transgene are highly resistant to necrosis induced by B. antracis lethal toxin (LeTx) while Casp1-heterozygous mice that are homozygous for the 129S1 Nlrp1b allele show a high susceptibility to necrosis from LeTx

hematopoietic system

abnormal macrophage physiology ( J:99748 )

Allelic Composition	Casp1^tm1Sesh/Casp1^tm1Sesh Nlrp1a^Neut1/Nlrp1a^Neut1
Genetic Background	involves: 129S2/SvPas * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Casp1^tm1Sesh mutation (5 available); any Casp1 mutation (42 available)
Nlrp1a^Neut1 mutation (0 available); any Nlrp1a mutation (64 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

immune system

immune system phenotype ( J:191055 )

N	• no neutrophilia or inflammatory disease • no loss of macrophage progenitor cells

increased circulating interleukin-18 level ( J:191055 )

homeostasis/metabolism

increased circulating interleukin-18 level ( J:191055 )

Allelic Composition	Casp1^tm1Sesh/Casp1⁺ Casp4^del/Casp4⁺
Genetic Background	involves: 129S2/SvPas * C57BL/6

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

immune system

decreased interleukin-1 beta secretion ( J:22964 )

• heterozygotes are slightly impaired in their capacity to produce mature IL-1beta: ex vivo, heterozygous peritoneal macrophages stimulated with LPS and ATP release 50% of wild-type IL-1beta levels

• no decrease in pro-IL-1beta synthesis or release is detected

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

neoplasm

neoplasm ( J:22964 , J:40691 )

N	• homozygotes are viable and healthy with no signs of histological abnormalities in major organs; no spontaneous tumors are detected until the age of 25 weeks (J:22964) • homozygotes remain tumor-free at the age of 18 months (J:40691)

cellular

cellular phenotype ( J:22964 , J:40691 )

• macrophages and thymocytes from mutant mice retain their capacity to undergo apoptosis upon ex vivo stimulation by several different signals (J:22964)

• in response to ATP, mutant peritoneal macrophages undergo normal apoptosis relative to wild-type (J:40691)

• in response to dexamethasone, aging or gamma irradiation, thymocytes from young homozygotes undergo normal apoptosis relative to wild-type (J:40691)

• in response to LPS and D-galactosamine, homozygotes undergo normal TNF-induced hepatocyte apoptosis and show normal kinetics of death from hepatic failure relative to wild-type mice (J:40691)

abnormal apoptosis ( J:80568 )

• mutant peripheral blood neutrophils display retarded constitutive apoptosis relative to wild-type neutrophils

• mutant peripheral blood neutrophils show no LPS-mediated inhibition of apoptosis but remain susceptible to Fas-mediated apoptosis

decreased T cell apoptosis ( J:40691 )

• in vitro, thymocytes from young homozygotes are resistant to Fas-induced apoptosis as measured by cell viability

decreased neuron apoptosis ( J:88212 )

• cultured cerebrocortical neurons from homozygotes are highly resistant to oxygen/glucose deprivation (OGD)-induced neuronal cell death, showing only 50% of lactate dehydrogenase release relative to wild-type neurons

• also, mutant neurons are highly resistant to Ripk2-mediated cell death; transfecting caspase-1 into mutant neurons restores sensitivity to Ripk2-induced apoptosis

• notably, cultured neurons show inhibition of OGD-mediated processing of various members of the caspase pathway, cleavage of Bid, and hypoxia-associated loss of mitochondrial transmembrane potential; in vivo, these findings are confirmed in a cerebral ischemia model

abnormal cell migration ( J:68644 )

• in homozygotes lacking bioactive IL-1beta, IL-18 fails to induce the expected migration of epidermal Langerhans cells to draining lymph nodes following skin sensitization; as a result, immunostimulatory dendritic cells fail to accumulate in regional lymph nodes resulting in impaired initiation of cutaneous immune responses

hematopoietic system

hematopoietic system phenotype ( J:22964 )

N	• homozygotes exhibit normal numbers of leukocytes, erythrocytes, and platelets in peripheral blood • freshly isolated mutant thymuses, spleens and lymph nodes contain a normal % of various T cell subsets and B cells relative to wild-type

decreased T cell apoptosis ( J:40691 )

• in vitro, thymocytes from young homozygotes are resistant to Fas-induced apoptosis as measured by cell viability

abnormal neutrophil physiology ( J:80568 )

• in addition to delayed apoptosis, mutant neutrophils show absence of LPS-stimulated IL-1beta production relative to wild-type

• in response to LPS-mediated acute lung injury, homozygotes show significantly increased total and percent neutrophil counts at 24 and 48 h; however, these numbers decline to wild-type levels by 72 h suggesting a delay in inflammatory neutrophil apoptosis

abnormal macrophage physiology ( J:22964 )

• ex vivo, thioglycollate-elicited peritoneal macrophages stimulated with LPS and ATP are defective in IL-1beta processing and release

immune system

immune system phenotype ( J:40691 )

N	• in homozygotes, the % of B lymphocytes and the various T lymphocyte subsets found in mutant thymuses, spleens and lymph nodes appear unaffected relative to wild-type • the size and lymphocyte counts in these lymphoid organs appear normal; myeolopoiesis remains unaffected

decreased T cell apoptosis ( J:40691 )

• in vitro, thymocytes from young homozygotes are resistant to Fas-induced apoptosis as measured by cell viability

abnormal neutrophil physiology ( J:80568 )

• in addition to delayed apoptosis, mutant neutrophils show absence of LPS-stimulated IL-1beta production relative to wild-type

abnormal macrophage physiology ( J:22964 )

• ex vivo, thioglycollate-elicited peritoneal macrophages stimulated with LPS and ATP are defective in IL-1beta processing and release

decreased circulating interleukin-1 alpha level ( J:22964 )

• LPS-treated mice show a 5-fold decrease in IL-1alpha levels in vivo

decreased circulating interleukin-1 beta level ( J:22964 )

• in vivo, homozygous males injected with a high dose of LPS display undetectable levels of mature IL-1beta in their plasma; females are slightly less affected

decreased circulating interleukin-6 level ( J:22964 )

• after injection with a high dose of LPS, homozygotes display a moderate reduction in IL-6 levels relative to wild-type mice

decreased circulating tumor necrosis factor level ( J:22964 )

• after injection with a high dose of LPS, homozygotes display a moderate reduction in TNF levels relative to wild-type mice

decreased interleukin-1 alpha secretion ( J:22964 )

• surprisingly, homozygous males are also defective in IL-1alpha production, with macrophages releasing only 20-25% of wild-type IL-1alpha levels after stimulation with LPS and ATP ex vivo

decreased interleukin-1 beta secretion ( J:22964 , J:88212 )

• homozygotes are impaired in their capacity to produce mature IL-1beta (J:22964)

• ex vivo, mutant peritoneal macrophages stimulated with LPS and ATP release less that 1% of wild-type IL-1beta levels; however, no decrease in pro-IL-1beta synthesis or release is detected (J:22964)

• in culture, mutant cortical neurons exhibit inhibition of hypoxia-mediated generation of mature IL-1beta (J:88212)

abnormal inflammatory response ( J:80568 )

• in response to LPS-mediated acute lung injury, homozygotes exhibit a prolonged neutrophilic inflammatory response and evidence of caspase-1-independent IL-1beta production in the lung

decreased susceptibility to endotoxin shock ( J:22964 , J:40691 )

• strikingly, homozygotes are significantly resistant to the lethal effects of endotoxic shock after a high dose of LPS (J:22964)

• whereas all LPS-treated wild-type mice die within 30 hours after injection, all homozygotes survive for >45 hours, with only 30% of mutants dying during the next 5 days (J:22964)

reproductive system

reproductive system phenotype ( J:22964 , J:40691 )

N	• homozygotes are fertile and produce a normal litter size relative to wild-type (J:22964) • in addition, post-lactation involution of mammary glands remains grossly normal in mutant post-partum females (J:22964) (J:40691)

nervous system

decreased neuron apoptosis ( J:88212 )

• also, mutant neurons are highly resistant to Ripk2-mediated cell death; transfecting caspase-1 into mutant neurons restores sensitivity to Ripk2-induced apoptosis

decreased susceptibility to ischemic brain injury ( J:69589 , J:98866 )

• under mild lesioning conditions (right carotid ligation plus 40 min 10% O2), newborn homozygotes show attenuated hypoxia-ischemia induced CCL2 (chemokine (C-C motif) ligand 2; also, MCP-1) expression at 8 h post-hypoxia relative to wild-type; no genotype differences in CCL2 production are observed in animals undergoing longer periods of hypoxia-ischemia (severe insult) (J:69589)

• following right carotid artery ligation, newborn homozygotes (P9-P10) are resistant to moderate, but not to severe cerebral hypoxic-ischemic insults relative to wild-type mice (J:98866)

homeostasis/metabolism

decreased circulating interleukin-1 alpha level ( J:22964 )

• LPS-treated mice show a 5-fold decrease in IL-1alpha levels in vivo

decreased circulating interleukin-1 beta level ( J:22964 )

• in vivo, homozygous males injected with a high dose of LPS display undetectable levels of mature IL-1beta in their plasma; females are slightly less affected

decreased circulating interleukin-6 level ( J:22964 )

• after injection with a high dose of LPS, homozygotes display a moderate reduction in IL-6 levels relative to wild-type mice

decreased circulating tumor necrosis factor level ( J:22964 )

• after injection with a high dose of LPS, homozygotes display a moderate reduction in TNF levels relative to wild-type mice

decreased susceptibility to ischemic brain injury ( J:69589 , J:98866 )

• following right carotid artery ligation, newborn homozygotes (P9-P10) are resistant to moderate, but not to severe cerebral hypoxic-ischemic insults relative to wild-type mice (J:98866)

cardiovascular system

cardiovascular system phenotype ( J:107324 )

N	• mice exhibit normal response to carotid ligation

Allelic Composition	Casp1^tm1Sesh/Casp1^tm1Sesh Casp4^del/Casp4^del Tg(Casp4)#Gne/0
Genetic Background	involves: 129S2/SvPas * C57BL/6 * NOD/ShiLtJ

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

immune system

decreased macrophage apoptosis ( J:193522 )

• impaired cell death in response to ATP and Clostridium difficile toxin B

decreased circulating interleukin-1 beta level ( J:193522 )

• in response to LPS challenge in a model of acute septic shock

decreased circulating interleukin-18 level ( J:193522 )

• in response to LPS challenge in a model of acute septic shock

decreased interleukin-1 alpha secretion ( J:193522 )

• from LPS-primed bone marrow-derived macrophage in response to ATP and C. difficile

• however, IL1a secretion is restored in response to CTB and E. coli

decreased interleukin-1 beta secretion ( J:193522 )

• LPS-primed bone marrow-derived macrophages fail to produce IL1b and IL18 in response to ATP, Clostridium difficile toxin B, cholera toxin B (CTB) or E. coli unlike controls

decreased interleukin-18 secretion ( J:193522 )

• LPS-primed bone marrow-derived macrophages fail to produce IL1b and IL18 in response to ATP, Clostridium difficile toxin B, cholera toxin B (CTB) or E. coli unlike controls

decreased susceptibility to endotoxin shock ( J:193522 )

• mice treated with LPS challenge in a model of acute septic shock exhibit reduced serum levels of IL1b and IL18 compared with controls

• however, mice do not survive beyond 26 hours and serum levels of IL1a are increased

homeostasis/metabolism

decreased circulating interleukin-1 beta level ( J:193522 )

• in response to LPS challenge in a model of acute septic shock

decreased circulating interleukin-18 level ( J:193522 )

• in response to LPS challenge in a model of acute septic shock

cellular

decreased macrophage apoptosis ( J:193522 )

• impaired cell death in response to ATP and Clostridium difficile toxin B

hematopoietic system

decreased macrophage apoptosis ( J:193522 )

• impaired cell death in response to ATP and Clostridium difficile toxin B

Allelic Composition	Casp1^tm1Sesh/Casp1^tm1Sesh Casp4^del/Casp4^del Slc11a1^r/Slc11a1^s
Genetic Background	involves: 129/Sv * 129S2/SvPas * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Casp1^tm1Sesh mutation (5 available); any Casp1 mutation (42 available)
Casp4^del mutation (5 available); any Casp4 mutation (33 available)
Slc11a1^r mutation (2 available); any Slc11a1 mutation (40 available)
Slc11a1^s mutation (0 available); any Slc11a1 mutation (40 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

immune system

increased susceptibility to bacterial infection ( J:112400 )

• mice succumb to 2x10¹⁰ CFU Salmonella infection with a median survival of 20 days compared to no death by infection for the control mice

Allelic Composition	Casp1^tm1Sesh/Casp1^tm1Sesh Casp4^del/Casp4^del
Genetic Background	NOD.129S2(B6)-Casp1^tm1Sesh Casp4^del/LtJ

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

immune system

decreased interleukin-1 alpha secretion ( J:87250 )

• cultured LPS-stimulated bone marrow derived macrophages from homozygous mutants secrete 20%-30% less IL-1alpha relative to heterozygous or wild-type (NOD/Lt) mice

decreased interleukin-1 beta secretion ( J:87250 )

• cultured LPS-stimulated bone marrow derived macrophages from homozygous mutants secrete 4-fold less IL-1beta relative to heterozygous or wild-type (NOD/Lt) mice

decreased interleukin-18 secretion ( J:87250 )

• cultured LPS-stimulated bone marrow derived macrophages from homozygotes produce no immunoreactive IL18 relative to heterozygous or wild-type (NOD/Lt) mice

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:87250 )

• homozygotes show no significant differences in the rate or in total incidence of diabetes relative to heterozygotes or wild-type (NOD/Lt) control mice

• weanling homozygotes injected with Complete Freund's adjuvant and young pre-diabetic males treated with multiple low dose streptozotocin behave similarly to control (wild-type, heterozygous, or NOD/Lt) mice

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
type 1 diabetes mellitus		DOID:9744	OMIM:222100	J:87250

Contributing Projects: Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
Citing These Resources Funding Information Warranty Disclaimer, Privacy Notice, Licensing, & Copyright Send questions and comments to User Support.	last database update 12/17/2024 MGI 6.24