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nox2 y nox2 null mice  (Jackson Laboratory)

 
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    Jackson Laboratory nox2 y nox2 null mice
    Comparison of ex vivo and in vivo vascular responses to angiotensin II acute treatment in wild-type or ‘redox-dead’ Cys17Ser PKARIα knock-in mice. A. Disulfide-PKARIα protein expression in thoracic aortae rings of WT or PKA KI mice subjected either to vehicle, AngII or H 2 O 2 for 5 min (n = 3). B–C. Constriction of abdominal aortae rings from WT or PKARIα KI mice ( B ), or WT <t>or</t> <t>Nox2-null</t> mice ( C ) in response to a single bolus dose of AngII (n ≥ 7). D-E. Acute constriction of abdominal aortae rings from WT or PKA KI mice in response to a single bolus dose of AngII after a vehicle or Nox2-inhibitor GSK2795039 (25 μM, 30 min pre-incubation) pre-treatment ( D ), or a vehicle or Nox1/4-inhibitor GKT137831 (1 μM, 30 min pre-incubation) pre-treatment ( E ) (n ≥ 5). F. Constriction of mesenteric arteries from WT or PKA KI mice in response to a single bolus dose of AngII (n ≥ 5). G. Constriction of penetrating cerebral arterioles in anesthetized WT or PKA KI mice in response to a single bolus administration of AngII (50 μg/kg, i.v.) (n ≥ 7). ∗P< 0.05, ∗∗P< 0.01 vs. vehicle or respective WT. M, PKARIα monomer; D, PKARIα dimer; H 2 O 2 , hydrogen peroxide, acts a vasodilator; AngII, angiotensin II, acts as vasoconstrictor; WT, wild type; PKA KI, Cys17Ser PKARIα knock-in mice; Nox2-null, Nox2 knockout mice; OGB, Oregon Green 488 BAPTA-1, cell permeable calcium dye; Texas Red, dye labels blood vessels in the brain for visualization.
    Nox2 Y Nox2 Null Mice, supplied by Jackson Laboratory, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    nox2 y nox2 null mice - by Bioz Stars, 2026-08
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    1) Product Images from "A redox sensor in protein kinase A regulatory subunit Iα regulates vasodilation and protects against hypertension"

    Article Title: A redox sensor in protein kinase A regulatory subunit Iα regulates vasodilation and protects against hypertension

    Journal: Redox Biology

    doi: 10.1016/j.redox.2026.104136

    Comparison of ex vivo and in vivo vascular responses to angiotensin II acute treatment in wild-type or ‘redox-dead’ Cys17Ser PKARIα knock-in mice. A. Disulfide-PKARIα protein expression in thoracic aortae rings of WT or PKA KI mice subjected either to vehicle, AngII or H 2 O 2 for 5 min (n = 3). B–C. Constriction of abdominal aortae rings from WT or PKARIα KI mice ( B ), or WT or Nox2-null mice ( C ) in response to a single bolus dose of AngII (n ≥ 7). D-E. Acute constriction of abdominal aortae rings from WT or PKA KI mice in response to a single bolus dose of AngII after a vehicle or Nox2-inhibitor GSK2795039 (25 μM, 30 min pre-incubation) pre-treatment ( D ), or a vehicle or Nox1/4-inhibitor GKT137831 (1 μM, 30 min pre-incubation) pre-treatment ( E ) (n ≥ 5). F. Constriction of mesenteric arteries from WT or PKA KI mice in response to a single bolus dose of AngII (n ≥ 5). G. Constriction of penetrating cerebral arterioles in anesthetized WT or PKA KI mice in response to a single bolus administration of AngII (50 μg/kg, i.v.) (n ≥ 7). ∗P< 0.05, ∗∗P< 0.01 vs. vehicle or respective WT. M, PKARIα monomer; D, PKARIα dimer; H 2 O 2 , hydrogen peroxide, acts a vasodilator; AngII, angiotensin II, acts as vasoconstrictor; WT, wild type; PKA KI, Cys17Ser PKARIα knock-in mice; Nox2-null, Nox2 knockout mice; OGB, Oregon Green 488 BAPTA-1, cell permeable calcium dye; Texas Red, dye labels blood vessels in the brain for visualization.
    Figure Legend Snippet: Comparison of ex vivo and in vivo vascular responses to angiotensin II acute treatment in wild-type or ‘redox-dead’ Cys17Ser PKARIα knock-in mice. A. Disulfide-PKARIα protein expression in thoracic aortae rings of WT or PKA KI mice subjected either to vehicle, AngII or H 2 O 2 for 5 min (n = 3). B–C. Constriction of abdominal aortae rings from WT or PKARIα KI mice ( B ), or WT or Nox2-null mice ( C ) in response to a single bolus dose of AngII (n ≥ 7). D-E. Acute constriction of abdominal aortae rings from WT or PKA KI mice in response to a single bolus dose of AngII after a vehicle or Nox2-inhibitor GSK2795039 (25 μM, 30 min pre-incubation) pre-treatment ( D ), or a vehicle or Nox1/4-inhibitor GKT137831 (1 μM, 30 min pre-incubation) pre-treatment ( E ) (n ≥ 5). F. Constriction of mesenteric arteries from WT or PKA KI mice in response to a single bolus dose of AngII (n ≥ 5). G. Constriction of penetrating cerebral arterioles in anesthetized WT or PKA KI mice in response to a single bolus administration of AngII (50 μg/kg, i.v.) (n ≥ 7). ∗P< 0.05, ∗∗P< 0.01 vs. vehicle or respective WT. M, PKARIα monomer; D, PKARIα dimer; H 2 O 2 , hydrogen peroxide, acts a vasodilator; AngII, angiotensin II, acts as vasoconstrictor; WT, wild type; PKA KI, Cys17Ser PKARIα knock-in mice; Nox2-null, Nox2 knockout mice; OGB, Oregon Green 488 BAPTA-1, cell permeable calcium dye; Texas Red, dye labels blood vessels in the brain for visualization.

    Techniques Used: Comparison, Ex Vivo, In Vivo, Knock-In, Expressing, Incubation, Knock-Out



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    Jackson Laboratory nox2 y nox2 null mice
    Comparison of ex vivo and in vivo vascular responses to angiotensin II acute treatment in wild-type or ‘redox-dead’ Cys17Ser PKARIα knock-in mice. A. Disulfide-PKARIα protein expression in thoracic aortae rings of WT or PKA KI mice subjected either to vehicle, AngII or H 2 O 2 for 5 min (n = 3). B–C. Constriction of abdominal aortae rings from WT or PKARIα KI mice ( B ), or WT <t>or</t> <t>Nox2-null</t> mice ( C ) in response to a single bolus dose of AngII (n ≥ 7). D-E. Acute constriction of abdominal aortae rings from WT or PKA KI mice in response to a single bolus dose of AngII after a vehicle or Nox2-inhibitor GSK2795039 (25 μM, 30 min pre-incubation) pre-treatment ( D ), or a vehicle or Nox1/4-inhibitor GKT137831 (1 μM, 30 min pre-incubation) pre-treatment ( E ) (n ≥ 5). F. Constriction of mesenteric arteries from WT or PKA KI mice in response to a single bolus dose of AngII (n ≥ 5). G. Constriction of penetrating cerebral arterioles in anesthetized WT or PKA KI mice in response to a single bolus administration of AngII (50 μg/kg, i.v.) (n ≥ 7). ∗P< 0.05, ∗∗P< 0.01 vs. vehicle or respective WT. M, PKARIα monomer; D, PKARIα dimer; H 2 O 2 , hydrogen peroxide, acts a vasodilator; AngII, angiotensin II, acts as vasoconstrictor; WT, wild type; PKA KI, Cys17Ser PKARIα knock-in mice; Nox2-null, Nox2 knockout mice; OGB, Oregon Green 488 BAPTA-1, cell permeable calcium dye; Texas Red, dye labels blood vessels in the brain for visualization.
    Nox2 Y Nox2 Null Mice, supplied by Jackson Laboratory, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    In <t>NOX2-null</t> mice, connexin levels in atrium and in ventricle are not affected by exposure to intermittent hypoxia. Homogenates were prepared from atria ( a , b ) or ventricles ( c ) of NOX2-null mice exposed to room air (RA) or exposed to intermittent hypoxia (IH). Cx40 ( a ) and Cx43 ( b , c ) were detected by immunoblotting. Gels were loaded with equal amounts of total protein (10 μg for A, 1 μg for B,C) and were also blotted with antibodies directed against vinculin (as a loading control). Graphs show the amounts (mean ± SEM) of immunoreactive connexin in control (RA) and IH mice determined by densitometry (adjusted for vinculin and normalized to the mean control values). Representative blots are shown on the right. The abundances of Cx40 and Cx43 did not differ significantly between RA (black bars) and IH groups (grey bars; p > 0.05, Student’s t test). n = 3 for atrium; n = 3 for ventricle)
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    Comparison of ex vivo and in vivo vascular responses to angiotensin II acute treatment in wild-type or ‘redox-dead’ Cys17Ser PKARIα knock-in mice. A. Disulfide-PKARIα protein expression in thoracic aortae rings of WT or PKA KI mice subjected either to vehicle, AngII or H 2 O 2 for 5 min (n = 3). B–C. Constriction of abdominal aortae rings from WT or PKARIα KI mice ( B ), or WT or Nox2-null mice ( C ) in response to a single bolus dose of AngII (n ≥ 7). D-E. Acute constriction of abdominal aortae rings from WT or PKA KI mice in response to a single bolus dose of AngII after a vehicle or Nox2-inhibitor GSK2795039 (25 μM, 30 min pre-incubation) pre-treatment ( D ), or a vehicle or Nox1/4-inhibitor GKT137831 (1 μM, 30 min pre-incubation) pre-treatment ( E ) (n ≥ 5). F. Constriction of mesenteric arteries from WT or PKA KI mice in response to a single bolus dose of AngII (n ≥ 5). G. Constriction of penetrating cerebral arterioles in anesthetized WT or PKA KI mice in response to a single bolus administration of AngII (50 μg/kg, i.v.) (n ≥ 7). ∗P< 0.05, ∗∗P< 0.01 vs. vehicle or respective WT. M, PKARIα monomer; D, PKARIα dimer; H 2 O 2 , hydrogen peroxide, acts a vasodilator; AngII, angiotensin II, acts as vasoconstrictor; WT, wild type; PKA KI, Cys17Ser PKARIα knock-in mice; Nox2-null, Nox2 knockout mice; OGB, Oregon Green 488 BAPTA-1, cell permeable calcium dye; Texas Red, dye labels blood vessels in the brain for visualization.

    Journal: Redox Biology

    Article Title: A redox sensor in protein kinase A regulatory subunit Iα regulates vasodilation and protects against hypertension

    doi: 10.1016/j.redox.2026.104136

    Figure Lengend Snippet: Comparison of ex vivo and in vivo vascular responses to angiotensin II acute treatment in wild-type or ‘redox-dead’ Cys17Ser PKARIα knock-in mice. A. Disulfide-PKARIα protein expression in thoracic aortae rings of WT or PKA KI mice subjected either to vehicle, AngII or H 2 O 2 for 5 min (n = 3). B–C. Constriction of abdominal aortae rings from WT or PKARIα KI mice ( B ), or WT or Nox2-null mice ( C ) in response to a single bolus dose of AngII (n ≥ 7). D-E. Acute constriction of abdominal aortae rings from WT or PKA KI mice in response to a single bolus dose of AngII after a vehicle or Nox2-inhibitor GSK2795039 (25 μM, 30 min pre-incubation) pre-treatment ( D ), or a vehicle or Nox1/4-inhibitor GKT137831 (1 μM, 30 min pre-incubation) pre-treatment ( E ) (n ≥ 5). F. Constriction of mesenteric arteries from WT or PKA KI mice in response to a single bolus dose of AngII (n ≥ 5). G. Constriction of penetrating cerebral arterioles in anesthetized WT or PKA KI mice in response to a single bolus administration of AngII (50 μg/kg, i.v.) (n ≥ 7). ∗P< 0.05, ∗∗P< 0.01 vs. vehicle or respective WT. M, PKARIα monomer; D, PKARIα dimer; H 2 O 2 , hydrogen peroxide, acts a vasodilator; AngII, angiotensin II, acts as vasoconstrictor; WT, wild type; PKA KI, Cys17Ser PKARIα knock-in mice; Nox2-null, Nox2 knockout mice; OGB, Oregon Green 488 BAPTA-1, cell permeable calcium dye; Texas Red, dye labels blood vessels in the brain for visualization.

    Article Snippet: Nox2−/y (Nox2-null) mice were obtained from Jackson Laboratories [ , ].

    Techniques: Comparison, Ex Vivo, In Vivo, Knock-In, Expressing, Incubation, Knock-Out

    In NOX2-null mice, connexin levels in atrium and in ventricle are not affected by exposure to intermittent hypoxia. Homogenates were prepared from atria ( a , b ) or ventricles ( c ) of NOX2-null mice exposed to room air (RA) or exposed to intermittent hypoxia (IH). Cx40 ( a ) and Cx43 ( b , c ) were detected by immunoblotting. Gels were loaded with equal amounts of total protein (10 μg for A, 1 μg for B,C) and were also blotted with antibodies directed against vinculin (as a loading control). Graphs show the amounts (mean ± SEM) of immunoreactive connexin in control (RA) and IH mice determined by densitometry (adjusted for vinculin and normalized to the mean control values). Representative blots are shown on the right. The abundances of Cx40 and Cx43 did not differ significantly between RA (black bars) and IH groups (grey bars; p > 0.05, Student’s t test). n = 3 for atrium; n = 3 for ventricle)

    Journal: BMC Cell Biology

    Article Title: Intermittent hypoxia causes NOX2-dependent remodeling of atrial connexins

    doi: 10.1186/s12860-016-0117-5

    Figure Lengend Snippet: In NOX2-null mice, connexin levels in atrium and in ventricle are not affected by exposure to intermittent hypoxia. Homogenates were prepared from atria ( a , b ) or ventricles ( c ) of NOX2-null mice exposed to room air (RA) or exposed to intermittent hypoxia (IH). Cx40 ( a ) and Cx43 ( b , c ) were detected by immunoblotting. Gels were loaded with equal amounts of total protein (10 μg for A, 1 μg for B,C) and were also blotted with antibodies directed against vinculin (as a loading control). Graphs show the amounts (mean ± SEM) of immunoreactive connexin in control (RA) and IH mice determined by densitometry (adjusted for vinculin and normalized to the mean control values). Representative blots are shown on the right. The abundances of Cx40 and Cx43 did not differ significantly between RA (black bars) and IH groups (grey bars; p > 0.05, Student’s t test). n = 3 for atrium; n = 3 for ventricle)

    Article Snippet: Eight-week-old male C57BL/6 J mice or hemizygous gp91phox-/Y (B6.129SCybb tm1Din/J) mice (NOX2-null) (Jackson Laboratories, Bar Harbor, ME) were exposed to intermittent hypoxia (IH) with alternating 90-s cycles (21% FiO 2 followed by 6% FiO 2 , 20 cycles/h) during daylight for 12 h/for 6 weeks.

    Techniques: Western Blot, Control

    In NOX2-null mice, the abundance and sizes of Cx40- and Cx43-containing gap junctions are not altered in atria of mice exposed to intermittent hypoxia. Cx43 and Cx40 were localized by immunofluorescence in frozen sections of atria of NOX2-null mice treated with RA or IH. (A) Representative photomicrographs are shown for each of these tissues and conditions. Bar, 20 μm. (B) Graph depicts the quantitation of the abundance of Cx43- and Cx40-immunoreactivity in atrial samples. The abundances of Cx43 and Cx40 did not differ significantly between RA (black bars) and IH treated mice (grey bars; p >0.05, Student’s t test) . (C) Graph depicts the quantitation of the sizes of atrial Cx43- and Cx40-containing immunoreactive objects in these samples. The sizes of Cx43 or Cx40 immunoreactive particles did not differ significantly between RA (black bars) and IH treated mice (grey bars p >0.05, Student’s t test). n = 14 for all treatments

    Journal: BMC Cell Biology

    Article Title: Intermittent hypoxia causes NOX2-dependent remodeling of atrial connexins

    doi: 10.1186/s12860-016-0117-5

    Figure Lengend Snippet: In NOX2-null mice, the abundance and sizes of Cx40- and Cx43-containing gap junctions are not altered in atria of mice exposed to intermittent hypoxia. Cx43 and Cx40 were localized by immunofluorescence in frozen sections of atria of NOX2-null mice treated with RA or IH. (A) Representative photomicrographs are shown for each of these tissues and conditions. Bar, 20 μm. (B) Graph depicts the quantitation of the abundance of Cx43- and Cx40-immunoreactivity in atrial samples. The abundances of Cx43 and Cx40 did not differ significantly between RA (black bars) and IH treated mice (grey bars; p >0.05, Student’s t test) . (C) Graph depicts the quantitation of the sizes of atrial Cx43- and Cx40-containing immunoreactive objects in these samples. The sizes of Cx43 or Cx40 immunoreactive particles did not differ significantly between RA (black bars) and IH treated mice (grey bars p >0.05, Student’s t test). n = 14 for all treatments

    Article Snippet: Eight-week-old male C57BL/6 J mice or hemizygous gp91phox-/Y (B6.129SCybb tm1Din/J) mice (NOX2-null) (Jackson Laboratories, Bar Harbor, ME) were exposed to intermittent hypoxia (IH) with alternating 90-s cycles (21% FiO 2 followed by 6% FiO 2 , 20 cycles/h) during daylight for 12 h/for 6 weeks.

    Techniques: Immunofluorescence, Quantitation Assay