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

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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 (21 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 (26 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 (150 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 (24 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 (150 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 (41 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 (21 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 (19 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

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