All Phenotypes Tg(Myh11-icre/ERT2)1Soff MGI Mouse

About Help FAQ

Phenotypes associated with this allele

Allele Symbol
Allele Name
Allele ID

Tg(Myh11-icre/ERT2)1Soff
transgene insertion 1, Stefan Offermanns
MGI:3819270

Summary

21 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Cyb5r3^{tm1c(KOMP)Wtsi}/Cyb5r3^{tm1c(KOMP)Wtsi} Tg(Myh11-icre/ERT2)1Soff/0	B6.Cg-Cyb5r3^{tm1c(KOMP)Wtsi} Tg(Myh11-icre/ERT2)1Soff	MGI:6379024
cn2	Gucy1b1^tm1.2Frb/Gucy1b1^tm1.2Frb X/Tg(Myh11-icre/ERT2)1Soff	B6.Cg-Gucy1b1^tm1.2Frb Tg(Myh11-icre/ERT2)1Soff	MGI:5432120
cn3	Atf4^tm1.1Cmad/Atf4^tm1.1Cmad Tg(Myh11-icre/ERT2)1Soff/?	D2.Cg-Atf4^tm1.1Cmad Tg(Myh11-icre/ERT2)1Soff	MGI:5812899
cn4	Gt(ROSA)26Sor^tm2(ATF4)Myz/Gt(ROSA)26Sor^tm2(ATF4)Myz Tg(Myh11-icre/ERT2)1Soff/?	either: D2.Cg-Atf4^tm1.1Cmad Tg(Myh11-icre/ERT2)1Soff or B6.Cg-Atf4^tm1.1Cmad Tg(Myh11-icre/ERT2)1Soff	MGI:5812901
cn5	Acvrl1^tm2.1Spo/Acvrl1^tm2.1Spo Tg(Myh11-icre/ERT2)1Soff/0	involves: 129 * FVB/N	MGI:5775200
cn6	Apoe^tm1Unc/Apoe^tm1Unc Atic^{tm1c(EUCOMM)Hmgu}/Atic^{tm1c(EUCOMM)Hmgu} X/Tg(Myh11-icre/ERT2)1Soff	involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6J * C57BL/6N * FVB/N	MGI:7511826
cn7	Gna11^tm1Soff/Gna11^tm1Soff Gnaq^tm2Soff/Gnaq^tm2Soff X/Tg(Myh11-icre/ERT2)1Soff	involves: 129P2/OlaHsd * 129S7/SvEvBrd * FVB/N	MGI:3819271
cn8	Apoe^tm1Unc/Apoe^tm1Unc Svep1^{tm1c(EUCOMM)Hmgu}/Svep1^{tm1c(EUCOMM)Hmgu} Tg(Myh11-icre/ERT2)1Soff/0	involves: 129P2/OlaHsd * C57BL/6N * FVB/N	MGI:7516351
cn9	Eng^tm2.1Hma/Eng^tm2.1Hma Tg(Myh11-icre/ERT2)1Soff/0	involves: 129P2/OlaHsd * FVB/N	MGI:5775198
cn10	Ano1^tm1.1Cahb/Ano1^tm1.1Cahb Tg(Myh11-icre/ERT2)1Soff/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N	MGI:5588166
cn11	Gna12^tm1Citb/Gna12^tm1Citb Gna13^tm2.1Soff/Gna13^tm2.1Soff X/Tg(Myh11-icre/ERT2)1Soff	involves: 129S1/Sv * FVB/N	MGI:3819345
cn12	Atic^{tm1c(EUCOMM)Hmgu}/Atic^{tm1c(EUCOMM)Hmgu} X/Tg(Myh11-icre/ERT2)1Soff	involves: 129S4/SvJaeSor * C57BL/6J * C57BL/6N * FVB/N	MGI:7511824
cn13	Kcnma1^tm1Ruth/Kcnma1^tm2.1Ruth X/Tg(Myh11-icre/ERT2)1Soff	involves: 129/Sv * C57BL/6 * FVB/N	MGI:3845037
cn14	Rgs2^tm1.1Kjb/Rgs2^tm1.1Kjb X/Tg(Myh11-icre/ERT2)1Soff	involves: 129X1/SvJ * C57BL/6 * FVB/N	MGI:5426419
cn15	Tg(ACTB-EGFP,-Kcnj8*G343D)9Nich/0 Tg(Myh11-icre/ERT2)1Soff/0	involves: C57BL/6 * CBA * FVB/N	MGI:6236323
cn16	Tg(ACTB-EGFP,-Kcnj8)1Nich/0 Tg(Myh11-icre/ERT2)1Soff/0	involves: C57BL/6 * CBA * FVB/N	MGI:6236322
cn17	Tg(ACTB-EGFP,-Kcnj8Q53RG343D)1Nich/0 Tg(Myh11-icre/ERT2)1Soff/0	involves: C57BL/6 * CBA * FVB/N	MGI:6236324
cn18	Arhgef1^tm1Rmt/Arhgef1^tm1Rmt X/Tg(Myh11-icre/ERT2)1Soff	involves: C57BL/6 * FVB/N	MGI:4442363
cn19	Ppp1r12a^em1Sfsh/Ppp1r12a⁺ Tg(Myh11-icre/ERT2)1Soff/0	involves: C57BL/6J * FVB/N	MGI:5776052
cn20	Tg(ACTB-EGFP,-Kcnj8*)1Wco/0 Tg(Myh11-icre/ERT2)1Soff/0	involves: FVB/N	MGI:6275077
cn21	Rgs4^tm1Sdlk/Rgs4^tm1Sdlk Tg(Myh11-icre/ERT2)1Soff/?	involves: FVB/N	MGI:5605986

Allelic Composition	Cyb5r3^{tm1c(KOMP)Wtsi}/Cyb5r3^{tm1c(KOMP)Wtsi} Tg(Myh11-icre/ERT2)1Soff/0
Genetic Background	B6.Cg-Cyb5r3^{tm1c(KOMP)Wtsi} Tg(Myh11-icre/ERT2)1Soff

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cyb5r3^{tm1c(KOMP)Wtsi} mutation (0 available); any Cyb5r3 mutation (19 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)

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

cardiovascular system

decreased heart rate ( J:280543 )

• heart rates are lower over a total 24 hour period in tamoxifen-induced mice

• tamoxifen-induced mice infused with angiotensin II show decreased heart rate compared to controls during the first 7 days of angiotensin treatment but while heart rate in wild-type mice declines between 8-9 days of angiotensin II, mutant mice maintain a consistent heart rate

increased susceptibility to hypertension ( J:280543 )

• mice are more susceptible to hypertensive agonists and have impaired ability to mitigate the effects of angiotensin II

increased mean systemic arterial blood pressure ( J:280543 )

• tamoxifen-induced mice exhibit a 5.84-mmHg increase in mean arterial pressure over a 24 hour period, with higher systolic and diastolic pressures

• tamoxifen-induced mice infused with angiotensin II to drive soluble guanylyl cyclase oxidation and elevate blood pressure exhibit a 14.75-mmHg blood pressure increase, with an increase in both mean arterial systolic and diastolic pressures

increased vasoconstriction ( J:280543 )

• hypertensive (via angiotensin II treatment) tamoxifen-induced mice show increased vasoconstriciton of mesenteric arteries in response to the thromboxane mimetic U46619

• however, vasoconstriction of non-angiotensin treated mesenteric arteries with U46619 shows no difference between wild-type and tamoxifen-treated mutant mice

decreased vasodilation ( J:280543 )

• tamoxifen-induced mice exhibit impaired acetylcholine-induced vasodilation in mesenteric arteries

• tamoxifen-induced mice exhibit a slight, but significant, impairment in vasodilation response of mesenteric arteries to BAY 58-2667, a soluble guanylyl cyclase heme-independent activator

• however, mice do not show differences in sodium nitroprusside, a nitric oxide donor molecule, induced vasodilation in mesenteric arteries

• tamoxifen-induced mice treated with angiotensin II to induce hypertension show impaired acetylcholine-mediated vasodilation

• hypertensive (via angiotensin II treatment) tamoxifen-induced mice exhibit diminished nitric oxide-dependent vasodilation in mesenteric arteries

• aortas from hypertensive tamoxifen-induced mice are less responsive to acetylcholine-mediated vasodilation

• however, aortas show no difference in phenylephrine-mediated vasoconstriction or vasodilation via SNP or BAY 58-2667

increased vasodilation ( J:280543 )

• hypertensive tamoxifen-induced mice exhibit increased vasodilation responsiveness to soluble guanylyl cyclase heme-independent activator BAY 58-2667

homeostasis/metabolism

increased physiological sensitivity to xenobiotic ( J:280543 )

• acute injection of BAY 58-2667 in angiotensin II-treated hypertensive tamoxifen-induced mice results in a greater blood pressure reduction than in controls

hematopoietic system

decreased monocyte cell number ( J:280543 )

• tamoxifen-induced mice exhibit fewer circulating monocytes compared to wild-type mice

• however, white blood cell, red blood cell, platelet, lymphocyte, and granulocyte counts are normal and hematocrit and hemoglobin levels are normal

immune system

decreased monocyte cell number ( J:280543 )

• tamoxifen-induced mice exhibit fewer circulating monocytes compared to wild-type mice

• however, white blood cell, red blood cell, platelet, lymphocyte, and granulocyte counts are normal and hematocrit and hemoglobin levels are normal

muscle

increased vasoconstriction ( J:280543 )

• hypertensive (via angiotensin II treatment) tamoxifen-induced mice show increased vasoconstriciton of mesenteric arteries in response to the thromboxane mimetic U46619

• however, vasoconstriction of non-angiotensin treated mesenteric arteries with U46619 shows no difference between wild-type and tamoxifen-treated mutant mice

decreased vasodilation ( J:280543 )

• tamoxifen-induced mice exhibit impaired acetylcholine-induced vasodilation in mesenteric arteries

• tamoxifen-induced mice exhibit a slight, but significant, impairment in vasodilation response of mesenteric arteries to BAY 58-2667, a soluble guanylyl cyclase heme-independent activator

• however, mice do not show differences in sodium nitroprusside, a nitric oxide donor molecule, induced vasodilation in mesenteric arteries

• tamoxifen-induced mice treated with angiotensin II to induce hypertension show impaired acetylcholine-mediated vasodilation

• hypertensive (via angiotensin II treatment) tamoxifen-induced mice exhibit diminished nitric oxide-dependent vasodilation in mesenteric arteries

• aortas from hypertensive tamoxifen-induced mice are less responsive to acetylcholine-mediated vasodilation

• however, aortas show no difference in phenylephrine-mediated vasoconstriction or vasodilation via SNP or BAY 58-2667

increased vasodilation ( J:280543 )

• hypertensive tamoxifen-induced mice exhibit increased vasodilation responsiveness to soluble guanylyl cyclase heme-independent activator BAY 58-2667

Allelic Composition	Gucy1b1^tm1.2Frb/Gucy1b1^tm1.2Frb X/Tg(Myh11-icre/ERT2)1Soff
Genetic Background	B6.Cg-Gucy1b1^tm1.2Frb Tg(Myh11-icre/ERT2)1Soff

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gucy1b1^tm1.2Frb mutation (0 available); any Gucy1b1 mutation (42 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)

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

cardiovascular system

abnormal systemic arterial blood pressure ( J:186053 )

• after more than 50 days of tamoxifen treatment, mice treated with L-NAME fail to exhibit an increase in systolic blood pressure compared with wild-type mice

hypertension ( J:186053 )

• in tamoxifen-treated mice

increased systemic arterial systolic blood pressure ( J:186053 )

• in tamoxifen-treated mice

decreased vasodilation ( J:186053 )

• after more than 50 days of tamoxifen treatment, mice lose aortic relaxation induced by NO, carbachol or sildenafil unlike control mice

• however, mice exhibit normal relaxation in response to 8-Br-cGMP or atrial natriuretic peptide

muscle

decreased vasodilation ( J:186053 )

• after more than 50 days of tamoxifen treatment, mice lose aortic relaxation induced by NO, carbachol or sildenafil unlike control mice

• however, mice exhibit normal relaxation in response to 8-Br-cGMP or atrial natriuretic peptide

Allelic Composition	Atf4^tm1.1Cmad/Atf4^tm1.1Cmad Tg(Myh11-icre/ERT2)1Soff/?
Genetic Background	D2.Cg-Atf4^tm1.1Cmad Tg(Myh11-icre/ERT2)1Soff

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atf4^tm1.1Cmad mutation (1 available); any Atf4 mutation (22 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)

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

cardiovascular system

abnormal aorta morphology ( J:237331 )

• following nephrectomy (to induce chronic kidney disease) and administration of tamoxifen, mice developed smaller calcified medial lesions than nephrectomized controls and similar to sham-operated controls

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:237331 )

N	• following nephrectomy (to induce chronic kidney disease) and administration of tamoxifen, levels of serum creatinine, phosphorus, calcium, cholesterol and triglyceride are similar to levels in nephrectomized wild-type mice

abnormal calcium ion homeostasis ( J:237331 )

• following nephrectomy (to induce chronic kidney disease) and administration of tamoxifen, aortic calcium content was lower than nephrectomized controls, but higher than sham-operated controls

Allelic Composition	Gt(ROSA)26Sor^tm2(ATF4)Myz/Gt(ROSA)26Sor^tm2(ATF4)Myz Tg(Myh11-icre/ERT2)1Soff/?
Genetic Background	either: D2.Cg-Atf4^tm1.1Cmad Tg(Myh11-icre/ERT2)1Soff or B6.Cg-Atf4^tm1.1Cmad Tg(Myh11-icre/ERT2)1Soff

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sor^tm2(ATF4)Myz mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)

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

cardiovascular system

calcified aorta ( J:237331 )

• following administration of tamoxifen, mice develop severe medial calcification in aortic sinuses

cellular

increased cardiomyocyte apoptosis ( J:237331 )

• following administration of tamoxifen, there is an increase of apoptotic cells in the aorta

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:237331 )

N	• following administration of tamoxifen, levels of phosphorus, calcium, cholesterol and triglyceride are similar to controls

muscle

increased cardiomyocyte apoptosis ( J:237331 )

• following administration of tamoxifen, there is an increase of apoptotic cells in the aorta

Allelic Composition	Acvrl1^tm2.1Spo/Acvrl1^tm2.1Spo Tg(Myh11-icre/ERT2)1Soff/0
Genetic Background	involves: 129 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Acvrl1^tm2.1Spo mutation (0 available); any Acvrl1 mutation (27 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)

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

cardiovascular system

cardiovascular system phenotype ( J:227170 )

N	• tamoxifen-treated mice do not develop arteriovenous (AV) shunts in any areas of the skin, including the wound areas

Allelic Composition	Apoe^tm1Unc/Apoe^tm1Unc Atic^{tm1c(EUCOMM)Hmgu}/Atic^{tm1c(EUCOMM)Hmgu} X/Tg(Myh11-icre/ERT2)1Soff
Genetic Background	involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6J * C57BL/6N * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoe^tm1Unc mutation (33 available); any Apoe mutation (158 available)
Atic^{tm1c(EUCOMM)Hmgu} mutation (0 available); any Atic mutation (35 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)

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

cardiovascular system

decreased susceptibility to atherosclerosis ( J:338121 )

• tamoxifen-treated mice fed a Western diet for 12 weeks show a significant decrease in atherosclerotic lesion size in whole aortas as well as smaller lesion areas and less lipid deposition in the aortic sinuses than similarly-fed control mice

• ACTA2 staining showed a significant reduction in the vascular smooth muscle cell (VSMC) content of atherosclerotic lesions in the aortic sinus

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:338121 )

N	• tamoxifen-treated mice fed a Western diet for 12 weeks show no significant differences in the level of plasma cholesterol, triglycerides, or glucose relative to controls

Allelic Composition	Gna11^tm1Soff/Gna11^tm1Soff Gnaq^tm2Soff/Gnaq^tm2Soff X/Tg(Myh11-icre/ERT2)1Soff
Genetic Background	involves: 129P2/OlaHsd * 129S7/SvEvBrd * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gna11^tm1Soff mutation (0 available); any Gna11 mutation (25 available)
Gnaq^tm2Soff mutation (0 available); any Gnaq mutation (24 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)

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

cardiovascular system

decreased systemic arterial blood pressure ( J:141641 )

• tamoxifen-treated mice exhibit decreased blood pressure following treatment with angiotensin II, vasopressin and endothelin compared to in wild-type mice

• tamoxifen-treated mice exposed to DOCA-salt do not develop hypertension and DOCA-salt treated mice exposed to tamoxifen following the onset of hypertension exhibit a drop in blood pressure compared to in similarly treated wild-type mice

decreased mean systemic arterial blood pressure ( J:141641 )

• following a normal transient increase in mean arterial blood pressure upon treatment with tamoxifen, mice exhibit a drop in mean arterial blood pressure below normal levels

• slight in the absence of tamoxifen induction

decreased vasoconstriction ( J:141641 )

• tamoxifen-treated mice fail to exhibit vasocontractile effects induced by phenylephrine or angiotensin II as do wild-type mice

• tamoxifen-treated mice exhibit reduced vasocontraction in response to serotonine, vasopressin, U46619 and endothelin-1 compared to similarly treated wild-type mice

muscle

decreased vasoconstriction ( J:141641 )

• tamoxifen-treated mice fail to exhibit vasocontractile effects induced by phenylephrine or angiotensin II as do wild-type mice

• tamoxifen-treated mice exhibit reduced vasocontraction in response to serotonine, vasopressin, U46619 and endothelin-1 compared to similarly treated wild-type mice

Allelic Composition	Apoe^tm1Unc/Apoe^tm1Unc Svep1^{tm1c(EUCOMM)Hmgu}/Svep1^{tm1c(EUCOMM)Hmgu} Tg(Myh11-icre/ERT2)1Soff/0
Genetic Background	involves: 129P2/OlaHsd * C57BL/6N * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoe^tm1Unc mutation (33 available); any Apoe mutation (158 available)
Svep1^{tm1c(EUCOMM)Hmgu} mutation (0 available); any Svep1 mutation (169 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)

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

cardiovascular system

abnormal artery morphology ( J:304349 )

• reduced atherosclerotic plaque burden in whole aorta and aortic arch and root after 8 and 16 weeks of HFD feeding

• reduced macrophage invasion of aortic atheromas and reduced necrotic core area after 8 and 16 weeks of HFD feeding

• increased atherosclerotic plaque collagen content after 16 weeks of HFD feeding

growth/size/body

growth/size/body region phenotype ( J:304349 )

N	• normal body weight after 8 and 16 weeks of HFD feeding

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:304349 )

N	• normal plasma total cholesterol, triglycerides and glucose levels after 8 weeks of HFD feeding • normal plasma total cholesterol and glucose levels after 16 weeks of HFD feeding

Allelic Composition	Eng^tm2.1Hma/Eng^tm2.1Hma Tg(Myh11-icre/ERT2)1Soff/0
Genetic Background	involves: 129P2/OlaHsd * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Eng^tm2.1Hma mutation (1 available); any Eng mutation (43 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)

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

cardiovascular system

cardiovascular system phenotype ( J:227170 )

N	• tamoxifen treated adults do not exhibit arteriovenous (AV) shunts in any areas of the skin including the wound areas

Allelic Composition	Ano1^tm1.1Cahb/Ano1^tm1.1Cahb Tg(Myh11-icre/ERT2)1Soff/0
Genetic Background	involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ano1^tm1.1Cahb mutation (0 available); any Ano1 mutation (60 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)

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

cardiovascular system

cardiovascular system phenotype ( J:207993 )

N	• tamoxifen-treated mice exhibit normal cardiac parameters (fractional shortening, cardiac output, ejection fraction, and heart rate)

abnormal pericyte morphology ( J:207993 )

• absent calcium-activated chloride currents in pericytes of small arterioles from brain, retina, skeletal muscle and skin of tamoxifen-treated mice

• almost absent U46619-induced depolarization in pericytes of tamoxifen-treated mice despite pericyte hyperpolarization after agonist application without a further increase upon replacement of chloride with methanesulfonate

abnormal vascular smooth muscle morphology ( J:207993 )

• vascular smooth muscle cells lack calcium-activated chloride currents in tamoxifen-treated mice

abnormal systemic arterial blood pressure ( J:207993 )

• decreased pressure amplitude in tamoxifen-treated mice

decreased mean systemic arterial blood pressure ( J:207993 )

• in tamoxifen-treated mice and more so in the presence of angiotensin II

• low-salt diet does not further decrease blood pressure

• however, systemic blood pressure differences are eliminated on a high-salt diet

abnormal blood vessel physiology ( J:207993 )

• reduced brain and retina small arteriole contractility in tamoxifen-treated mice

decreased vasoconstriction ( J:207993 )

• reduced vascular smooth muscle cell contractility in the aorta of tamoxifen-treated mice

• however, contractility in mesenteric arteries is normal

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:207993 )

N	• tamoxifen-treated mice exhibit normal plasma aldosterone, renin, angiotensin II, potassium and various blood gas parameters • tamoxifen-treated mice exhibit normal creatinine clearance and fractional excretion of sodium, chloride and potassium

muscle

abnormal vascular smooth muscle morphology ( J:207993 )

• vascular smooth muscle cells lack calcium-activated chloride currents in tamoxifen-treated mice

decreased vasoconstriction ( J:207993 )

• reduced vascular smooth muscle cell contractility in the aorta of tamoxifen-treated mice

• however, contractility in mesenteric arteries is normal

Allelic Composition	Gna12^tm1Citb/Gna12^tm1Citb Gna13^tm2.1Soff/Gna13^tm2.1Soff X/Tg(Myh11-icre/ERT2)1Soff
Genetic Background	involves: 129S1/Sv * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gna12^tm1Citb mutation (0 available); any Gna12 mutation (23 available)
Gna13^tm2.1Soff mutation (0 available); any Gna13 mutation (12 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)

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

cardiovascular system

decreased systemic arterial blood pressure ( J:141641 )

• tamoxifen-treated mice exhibit decreased blood pressure following treatment with U46619, vasopressin and endothelin compared to in wild-type mice

decreased vasoconstriction ( J:141641 )

• tamoxifen-treated mice exhibit reduced vasocontraction in response to angiotensin II, U46619 and endothelin-1 compared to in similarly treated wild-type mice

muscle

decreased vasoconstriction ( J:141641 )

• tamoxifen-treated mice exhibit reduced vasocontraction in response to angiotensin II, U46619 and endothelin-1 compared to in similarly treated wild-type mice

Allelic Composition	Atic^{tm1c(EUCOMM)Hmgu}/Atic^{tm1c(EUCOMM)Hmgu} X/Tg(Myh11-icre/ERT2)1Soff
Genetic Background	involves: 129S4/SvJaeSor * C57BL/6J * C57BL/6N * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atic^{tm1c(EUCOMM)Hmgu} mutation (0 available); any Atic mutation (35 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)

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

cardiovascular system

decreased vascular smooth muscle cell proliferation ( J:338121 )

• 21 days after left common carotid artery ligation, tamoxifen-treated mice show a significant reduction in the % of proliferating (EdU+) VSMCs in cross-sections of arterial neointima relative to control mice

• expression of the proliferative marker PCNA is significantly reduced in ligated arteries 7 days after injury

abnormal vascular wound healing ( J:338121 )

• 21 days after left common carotid artery ligation, tamoxifen-treated mice show a significant reduction in the neointima area and neointima/medial area ratio in sections 200 to 600 um from the site of ligation relative to control mice

• however, the external elastic lamina circumference of ligated carotid artery is similar to that in control mice, indicating that vascular constrictive remodeling is unaffected

cellular

decreased vascular smooth muscle cell proliferation ( J:338121 )

• expression of the proliferative marker PCNA is significantly reduced in ligated arteries 7 days after injury

homeostasis/metabolism

abnormal vascular wound healing ( J:338121 )

• however, the external elastic lamina circumference of ligated carotid artery is similar to that in control mice, indicating that vascular constrictive remodeling is unaffected

muscle

decreased vascular smooth muscle cell proliferation ( J:338121 )

• expression of the proliferative marker PCNA is significantly reduced in ligated arteries 7 days after injury

Allelic Composition	Kcnma1^tm1Ruth/Kcnma1^tm2.1Ruth X/Tg(Myh11-icre/ERT2)1Soff
Genetic Background	involves: 129/Sv * C57BL/6 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Kcnma1^tm1Ruth mutation (0 available); any Kcnma1 mutation (101 available)
Kcnma1^tm2.1Ruth mutation (0 available); any Kcnma1 mutation (101 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)

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

renal/urinary system

abnormal urinary bladder physiology ( J:148424 )

• the iberiotoxin sensitive component of the large noninactivating outward currents induced in urinary bladder smooth muscle cells by membrane depolarization is absent after tamoxifen treatment

• following tamoxifen treatment, peak contractions are more accentuated and maximal contraction is seen at lower electric field stimulation frequencies in detrusor muscle strips with intact urothelium

• following tamoxifen treatment, peak contractions of detrusor muscle strips with intact urothelium are stronger at stimulation frequencies of 1, 2, and 4 Hz compared to mice homozygous for Kcnma1^tm1Ruth

increased urination frequency ( J:148424 )

• following tamoxifen treatment, an increase in the number of micturitions following intake of a defined amount of fluid is seen compared to both wild-type mice and mice homozygous for Kcnma1^tm1Ruth

muscle

abnormal muscle contractility ( J:148424 )

• following tamoxifen treatment, urinary bladder detrusor muscle is more sensitive to isoproterenol and Sp-5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole-3',5'-monophosphorothioate induced inhibition of contractility compared to controls

Allelic Composition	Rgs2^tm1.1Kjb/Rgs2^tm1.1Kjb X/Tg(Myh11-icre/ERT2)1Soff
Genetic Background	involves: 129X1/SvJ * C57BL/6 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rgs2^tm1.1Kjb mutation (0 available); any Rgs2 mutation (21 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)

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

cardiovascular system

cardiovascular system phenotype ( J:184284 )

N	• treatment with tamoxifen has an insignificant affect on either acetyl choline or sodium nitroprusside induced dilation of mesenteric arteries relative to controls

Allelic Composition	Tg(ACTB-EGFP,-Kcnj8*G343D)9Nich/0 Tg(Myh11-icre/ERT2)1Soff/0
Genetic Background	involves: C57BL/6 * CBA * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(ACTB-EGFP,-Kcnj8*G343D)9Nich mutation (0 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)

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

cardiovascular system

hypotension ( J:202037 )

• systolic and diastolic blood pressures are lower 3 weeks following tamoxifen induction

• however, heart rate is not affected

abnormal vascular smooth muscle physiology ( J:202037 )

• in vascular smooth muscle cells (VSMC), potassium currents are higher than in control VSMCs under basal conditions and with the K(ATP) channel opener, pinacidil, indicating enhanced K(ATP) channel currents

decreased vasoconstriction ( J:202037 )

• contraction of mesenteric arteries in response to phenylephrine is shifted about 10-fold to higher phenylephrine concentration compared to control arteries , with an even greater relative shift in the presence of pinacidil, indicating reduced contractility of blood vessels

• however, following constriction by high phenylephrine concentration, subsequent K(ATP)-independent relaxation in response to sodium nitroprusside is not different

muscle

abnormal vascular smooth muscle physiology ( J:202037 )

decreased vasoconstriction ( J:202037 )

• however, following constriction by high phenylephrine concentration, subsequent K(ATP)-independent relaxation in response to sodium nitroprusside is not different

Allelic Composition	Tg(ACTB-EGFP,-Kcnj8)1Nich/0 Tg(Myh11-icre/ERT2)1Soff/0
Genetic Background	involves: C57BL/6 * CBA * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(ACTB-EGFP,-Kcnj8)1Nich mutation (0 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)

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

cardiovascular system

cardiovascular system phenotype ( J:202037 )

N	• systolic and diastolic blood pressures are not affected 3 weeks following tamoxifen induction

Allelic Composition	Tg(ACTB-EGFP,-Kcnj8Q53RG343D)1Nich/0 Tg(Myh11-icre/ERT2)1Soff/0
Genetic Background	involves: C57BL/6 * CBA * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(ACTB-EGFP,-Kcnj8*Q53R*G343D)1Nich mutation (0 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)

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

cardiovascular system

hypotension ( J:202037 )

• systolic and diastolic blood pressures are lower 3 weeks following tamoxifen induction

• however, heart rate is not affected

Allelic Composition	Arhgef1^tm1Rmt/Arhgef1^tm1Rmt X/Tg(Myh11-icre/ERT2)1Soff
Genetic Background	involves: C57BL/6 * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Arhgef1^tm1Rmt mutation (0 available); any Arhgef1 mutation (73 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)

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

cardiovascular system

abnormal aorta wall morphology ( J:157074 )

• arterial wall remodeling in response to Angiotensin II treatment is absent

cardiac hypertrophy ( J:157074 )

• cardiac hypertrophy, as assessed by the heart to body weight ratio, is significantly reduced in mice treated with both tamoxifen and Angiotensin II

abnormal systemic arterial blood pressure ( J:157074 )

• Angiotensin II or N-nitro-l-arginine (L-NAME) treatment do not increase blood pressure in tamoxifen treated mice

• tamoxifen treatment starting 10 days after the beginning of Angiotensin II treatment is able to reverse Angiotensin II induced hypertension

• mice treated with deoxycorticosterone acetate plus NaCl are not completely protected from induced hypertension and are resistant to the blood pressure-lowering effects of the subsequent treatment with an Angiotensin II type 1 receptor antagonist

decreased vasoconstriction ( J:157074 )

• the amplitude of Angiotensin II induced contractions was much lower in the ex vivo aortic rings, from tamoxifen treated mice

• in tamoxifen treated mice the in vivo response to Angiotensin II is reduced

muscle

decreased vasoconstriction ( J:157074 )

• the amplitude of Angiotensin II induced contractions was much lower in the ex vivo aortic rings, from tamoxifen treated mice

• in tamoxifen treated mice the in vivo response to Angiotensin II is reduced

homeostasis/metabolism

decreased physiological sensitivity to xenobiotic ( J:157074 )

• N-nitro-l-arginine (L-NAME) does not induce hypertension in tamoxifen treated mice

growth/size/body

cardiac hypertrophy ( J:157074 )

• cardiac hypertrophy, as assessed by the heart to body weight ratio, is significantly reduced in mice treated with both tamoxifen and Angiotensin II

Allelic Composition	Ppp1r12a^em1Sfsh/Ppp1r12a⁺ Tg(Myh11-icre/ERT2)1Soff/0
Genetic Background	involves: C57BL/6J * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ppp1r12a^em1Sfsh mutation (1 available); any Ppp1r12a mutation (62 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)

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

cardiovascular system

abnormal blood vessel physiology ( J:230106 )

• tamoxifen-treated mice exhibit a 5-fold increase in sensitivity to 8-Br-cGMP under calcium clamp and increased maximal relaxation in mesenteric arteries compared with control mice

Allelic Composition	Tg(ACTB-EGFP,-Kcnj8*)1Wco/0 Tg(Myh11-icre/ERT2)1Soff/0
Genetic Background	involves: FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(ACTB-EGFP,-Kcnj8*)1Wco mutation (0 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)

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

cardiovascular system

hypertension ( J:202037 )

• mice exhibit an increase in blood pressure following tamoxifen treatment

Allelic Composition	Rgs4^tm1Sdlk/Rgs4^tm1Sdlk Tg(Myh11-icre/ERT2)1Soff/?
Genetic Background	involves: FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rgs4^tm1Sdlk mutation (1 available); any Rgs4 mutation (22 available)
Tg(Myh11-icre/ERT2)1Soff mutation (2 available)

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

mortality/aging

increased susceptibility to induced morbidity/mortality ( J:215588 )

• following 25 minute bilateral ischemic kidney injury (25BI), cumulative survival is decreased as compared to controls

hematopoietic system

abnormal macrophage chemotaxis ( J:215588 )

• increased numbers of macrophages localize to injured kidneys 18 hours after 10 minute unilateral kidney injury as compared to controls

homeostasis/metabolism

increased circulating creatinine level ( J:215588 )

• serum creatinine levels are increased 88% 48 hours after 25BI as compared to controls

immune system

abnormal macrophage chemotaxis ( J:215588 )

• increased numbers of macrophages localize to injured kidneys 18 hours after 10 minute unilateral kidney injury as compared to controls

cellular

abnormal macrophage chemotaxis ( J:215588 )

• increased numbers of macrophages localize to injured kidneys 18 hours after 10 minute unilateral kidney injury as compared to controls

renal/urinary system

abnormal renal tubule morphology ( J:215588 )

• tubular injury is more extensive 24 hours after 25BI as compared to controls

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 11/12/2024 MGI 6.24