Structured Review

The Jackson Laboratory wild type wt mice
Atrial Energetics and Mitochondrial Dysfunction in Mouse Model of Atrial Fibrillation with Heart Failure. A, B C) As opposed to <t>wild</t> <t>type</t> <t>(WT)</t> <t>mice,</t> a novel mouse model of atrial fibrillation (AF) shows significant electrical and structural remodeling. Electrocardiograms demonstrate sinus rhythm (SR) in wild type (WT) ( A ) and LKB1 knockout (KO) mice ( B ). LKB1 KO mice develop spontaneous AF ( C) and then heart failure (HF). Cardiac magnetic resonance imaging showed significant right and left atrial enlargement in LKB1 KO mice in AF and HF ( lower panel ). D) ECG analysis demonstrated heart rate was similar in WT and KO mice in SR while ventricular rate was slower in KO in AF and HF. E ). Atrial size significantly increased in AF and HF with progressive right and left atrial enlargement compare to WT mice. F ) Left ventricular ejection fraction was reduced in AF. G, H I ) Disrupted atrial energetics and metabolism was associated with development of atrial remodeling, AF and HF. Atrial myocardial content of nucleotides including ATP ( G ) and ADP ( H ) was significantly lower in LKB1 KO mice in SR and AF compare to WT mice. As shown by high performance liquid chromatography measurement ( G ), ATP was significantly depleted in LKB1 KO atrial myocardium starting in SR and further decrease in AF. Metabolic stress, as reflected in AMP/ATP ratio ( I ), was more significant in LKB1 KO hearts with AF than in WT. Thus, AF is associated with impaired myocardial energetics and metabolism. The immunoblot analysis is corrected with loading control, antibody against GAPDH. (* P
Wild Type Wt Mice, supplied by The Jackson Laboratory, used in various techniques. Bioz Stars score: 92/100, based on 250 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/wild type wt mice/product/The Jackson Laboratory
Average 92 stars, based on 250 article reviews
Price from $9.99 to $1999.99
wild type wt mice - by Bioz Stars, 2021-01
92/100 stars

Images

1) Product Images from "MOLECULAR MECHANISM OF THE ASSOCIATION BETWEEN ATRIAL FIBRILLATION AND HEART FAILURE INCLUDES ENERGY METABOLIC DYSREGULATION"

Article Title: MOLECULAR MECHANISM OF THE ASSOCIATION BETWEEN ATRIAL FIBRILLATION AND HEART FAILURE INCLUDES ENERGY METABOLIC DYSREGULATION

Journal: Journal of cardiac failure

doi: 10.1016/j.cardfail.2019.08.005

Atrial Energetics and Mitochondrial Dysfunction in Mouse Model of Atrial Fibrillation with Heart Failure. A, B C) As opposed to wild type (WT) mice, a novel mouse model of atrial fibrillation (AF) shows significant electrical and structural remodeling. Electrocardiograms demonstrate sinus rhythm (SR) in wild type (WT) ( A ) and LKB1 knockout (KO) mice ( B ). LKB1 KO mice develop spontaneous AF ( C) and then heart failure (HF). Cardiac magnetic resonance imaging showed significant right and left atrial enlargement in LKB1 KO mice in AF and HF ( lower panel ). D) ECG analysis demonstrated heart rate was similar in WT and KO mice in SR while ventricular rate was slower in KO in AF and HF. E ). Atrial size significantly increased in AF and HF with progressive right and left atrial enlargement compare to WT mice. F ) Left ventricular ejection fraction was reduced in AF. G, H I ) Disrupted atrial energetics and metabolism was associated with development of atrial remodeling, AF and HF. Atrial myocardial content of nucleotides including ATP ( G ) and ADP ( H ) was significantly lower in LKB1 KO mice in SR and AF compare to WT mice. As shown by high performance liquid chromatography measurement ( G ), ATP was significantly depleted in LKB1 KO atrial myocardium starting in SR and further decrease in AF. Metabolic stress, as reflected in AMP/ATP ratio ( I ), was more significant in LKB1 KO hearts with AF than in WT. Thus, AF is associated with impaired myocardial energetics and metabolism. The immunoblot analysis is corrected with loading control, antibody against GAPDH. (* P
Figure Legend Snippet: Atrial Energetics and Mitochondrial Dysfunction in Mouse Model of Atrial Fibrillation with Heart Failure. A, B C) As opposed to wild type (WT) mice, a novel mouse model of atrial fibrillation (AF) shows significant electrical and structural remodeling. Electrocardiograms demonstrate sinus rhythm (SR) in wild type (WT) ( A ) and LKB1 knockout (KO) mice ( B ). LKB1 KO mice develop spontaneous AF ( C) and then heart failure (HF). Cardiac magnetic resonance imaging showed significant right and left atrial enlargement in LKB1 KO mice in AF and HF ( lower panel ). D) ECG analysis demonstrated heart rate was similar in WT and KO mice in SR while ventricular rate was slower in KO in AF and HF. E ). Atrial size significantly increased in AF and HF with progressive right and left atrial enlargement compare to WT mice. F ) Left ventricular ejection fraction was reduced in AF. G, H I ) Disrupted atrial energetics and metabolism was associated with development of atrial remodeling, AF and HF. Atrial myocardial content of nucleotides including ATP ( G ) and ADP ( H ) was significantly lower in LKB1 KO mice in SR and AF compare to WT mice. As shown by high performance liquid chromatography measurement ( G ), ATP was significantly depleted in LKB1 KO atrial myocardium starting in SR and further decrease in AF. Metabolic stress, as reflected in AMP/ATP ratio ( I ), was more significant in LKB1 KO hearts with AF than in WT. Thus, AF is associated with impaired myocardial energetics and metabolism. The immunoblot analysis is corrected with loading control, antibody against GAPDH. (* P

Techniques Used: Mouse Assay, Knock-Out, Magnetic Resonance Imaging, High Performance Liquid Chromatography

Mitochondrial Dysfunction in mechanism of Atrial Fibrillation and Heart Failure in Mice Atria. A-F) Mitochondrial electron transport chain, matrix, inner- and outer membrane proteins were significantly impaired in LKB1 knockout (KO) heart atria compared with wild type (WT) atria, particularly in atrial fibrillation (AF) and heart failure (HF) co-existence. In KO atria with AF and HF, succinate dehydrogenase (complex II) ( A ), cytochrome c oxidase (complex IV) ( B ), pyruvate dehydrogenase ( C ), voltage gated anion channel ( D ), prohibitins 1 ( E ) and cytochrome c ( F ) levels were significantly lower compare to WT atria and KO atria in sinus rhythm (SR) without HF. Functional and structural impairment started in SR and then worsen in persAF and HF. G-I) Mitochondrial dysfunction was associated with oxidative stress and mitochondrial DNA (mtDNA) damage. There was significantly higher reactive oxygen species (ROS) generation in AF and HF compared to WT atrial tissue as shown in elevated level of hydrogen peroxide (H 2 O 2 ) that was measured by using 2,7-dichlorofluorescein (DCF) diacetate fluorescence ( G ) and superoxide as shown elevated ROS scavenger, superoxide dismutase (SOD) ( H ). Mitochondrial DNA (mtDNA, long fragment: 8636-bp) was significantly damaged in AF and HF ( I, upper panel ). However, the short fragment of mtDNA was similarly amplified in both groups ( I, lower panel ). Thus, impaired mitochondrial complexes and oxidative stress were associated with mtDNA damage in AF and HF. Insets show western blotting for specific proteins in panels A-F and H. The immunoblot analysis is corrected with loading control, antibody against GAPDH. (* P
Figure Legend Snippet: Mitochondrial Dysfunction in mechanism of Atrial Fibrillation and Heart Failure in Mice Atria. A-F) Mitochondrial electron transport chain, matrix, inner- and outer membrane proteins were significantly impaired in LKB1 knockout (KO) heart atria compared with wild type (WT) atria, particularly in atrial fibrillation (AF) and heart failure (HF) co-existence. In KO atria with AF and HF, succinate dehydrogenase (complex II) ( A ), cytochrome c oxidase (complex IV) ( B ), pyruvate dehydrogenase ( C ), voltage gated anion channel ( D ), prohibitins 1 ( E ) and cytochrome c ( F ) levels were significantly lower compare to WT atria and KO atria in sinus rhythm (SR) without HF. Functional and structural impairment started in SR and then worsen in persAF and HF. G-I) Mitochondrial dysfunction was associated with oxidative stress and mitochondrial DNA (mtDNA) damage. There was significantly higher reactive oxygen species (ROS) generation in AF and HF compared to WT atrial tissue as shown in elevated level of hydrogen peroxide (H 2 O 2 ) that was measured by using 2,7-dichlorofluorescein (DCF) diacetate fluorescence ( G ) and superoxide as shown elevated ROS scavenger, superoxide dismutase (SOD) ( H ). Mitochondrial DNA (mtDNA, long fragment: 8636-bp) was significantly damaged in AF and HF ( I, upper panel ). However, the short fragment of mtDNA was similarly amplified in both groups ( I, lower panel ). Thus, impaired mitochondrial complexes and oxidative stress were associated with mtDNA damage in AF and HF. Insets show western blotting for specific proteins in panels A-F and H. The immunoblot analysis is corrected with loading control, antibody against GAPDH. (* P

Techniques Used: Mouse Assay, Knock-Out, Functional Assay, Fluorescence, Amplification, Western Blot

Mitochondrial Ultrastructural Remodeling in Mechanism of Atrial Fibrillation and Heart Failure. A-F) Mitochondrial ultrastructure was significantly disrupted in atrial fibrillation (AF) and heart failure (HF). Electron microscopy showed that atrial cardiomyocyte with AF and HF has higher number of mitochondria than in wild type (WT) ( A ) and larger mitochondrion-volume ( B ). Mitochondrial matrix edema and disruption of the inner and outer membranes were demonstrated by measurement of crista density that was significantly lower in AF and HF indicating mitochondrial damage ( C ). Electron microscopy images showed significantly impaired mitochondrial ultrastructure in cardiomyocytes with AF compare to WT in SR ( D, E F ). Mitochondrial functional and structural damage were associated with activation of mitochondrial apoptotic cascade (caspase 9) in mice atria ( G ), and human atria ( H ) with HF and AF. Mitochondrial apoptotic cascade, was activated in KO atria in AF compare to WT atria. Insets show western blotting for specific proteins in panels G and H. The immunoblot analysis is corrected with loading control, antibody against GAPDH. (* P
Figure Legend Snippet: Mitochondrial Ultrastructural Remodeling in Mechanism of Atrial Fibrillation and Heart Failure. A-F) Mitochondrial ultrastructure was significantly disrupted in atrial fibrillation (AF) and heart failure (HF). Electron microscopy showed that atrial cardiomyocyte with AF and HF has higher number of mitochondria than in wild type (WT) ( A ) and larger mitochondrion-volume ( B ). Mitochondrial matrix edema and disruption of the inner and outer membranes were demonstrated by measurement of crista density that was significantly lower in AF and HF indicating mitochondrial damage ( C ). Electron microscopy images showed significantly impaired mitochondrial ultrastructure in cardiomyocytes with AF compare to WT in SR ( D, E F ). Mitochondrial functional and structural damage were associated with activation of mitochondrial apoptotic cascade (caspase 9) in mice atria ( G ), and human atria ( H ) with HF and AF. Mitochondrial apoptotic cascade, was activated in KO atria in AF compare to WT atria. Insets show western blotting for specific proteins in panels G and H. The immunoblot analysis is corrected with loading control, antibody against GAPDH. (* P

Techniques Used: Electron Microscopy, Functional Assay, Activation Assay, Mouse Assay, Western Blot

2) Product Images from "Endothelial exosome plays functional role during rickettsial infection"

Article Title: Endothelial exosome plays functional role during rickettsial infection

Journal: bioRxiv

doi: 10.1101/2020.11.16.385740

Recipient cells take up Exos. ( a ) Purified plsExos (5 x 10 10 particles in 50 μL PBS) labeled with PKH26 were administrated to wild-type mice intravenously (n=3). After 4 hrs, organs were dissected for frozen sectioning after euthanasia and perfusion via the right ventricle. Representative immunofluorescent staining of ECs from liver, brain, and lung using an antibody against CD31(an EC marker) is shown. The nuclei were stained with DAPI. Cells with red fluorescence indicate the uptake of PKH26 labeled Exos. Scale bars, 20 µm. ( b ) Purified ECExos were labeled with PKH26 (red) and added to the culture medium of human BMECs (2000 particles per cell) as indicated. Pictures were taken using fluorescence microscopy after 2 hrs of ECExo incubation. Scale bars, 20 µm.
Figure Legend Snippet: Recipient cells take up Exos. ( a ) Purified plsExos (5 x 10 10 particles in 50 μL PBS) labeled with PKH26 were administrated to wild-type mice intravenously (n=3). After 4 hrs, organs were dissected for frozen sectioning after euthanasia and perfusion via the right ventricle. Representative immunofluorescent staining of ECs from liver, brain, and lung using an antibody against CD31(an EC marker) is shown. The nuclei were stained with DAPI. Cells with red fluorescence indicate the uptake of PKH26 labeled Exos. Scale bars, 20 µm. ( b ) Purified ECExos were labeled with PKH26 (red) and added to the culture medium of human BMECs (2000 particles per cell) as indicated. Pictures were taken using fluorescence microscopy after 2 hrs of ECExo incubation. Scale bars, 20 µm.

Techniques Used: Purification, Labeling, Mouse Assay, Staining, Marker, Fluorescence, Microscopy, Incubation

Related Articles

Knock-Out:

Article Title: MOLECULAR MECHANISM OF THE ASSOCIATION BETWEEN ATRIAL FIBRILLATION AND HEART FAILURE INCLUDES ENERGY METABOLIC DYSREGULATION
Article Snippet: .. Cardiac specific liver kinase B1 (LKB1) knockout (KO) mice ( C57BL/6 ) were generated by crossing LKB1 flox/flox mice with transgenic mice expressing Cre-recombinase from the myosin heavy chain promoter., , LKB1 KO mice were born in SR and then developed spontaneous AF which followed with HF in persAF as we and others reported previously., , Wild-type (WT) mice were of the same strain as the corresponding transgenic mice (Jackson Lab). ..

Article Title: The Absence of Indoleamine 2,3-Dioxygenase Inhibits Retinal Capillary Degeneration in Diabetic Mice
Article Snippet: .. IDO knockout (IDO−/− ) and wild-type (WT) mice (all on C57BL/6J background) were obtained from Jackson Laboratories (Bar Harbor, ME, USA). .. Male IDO−/− and WT mice at 3 months of age were administered five sequential intraperitoneal injections of streptozotocin (MP Biomedicals, Solon, OH, USA) solution freshly prepared in citrate buffer (pH 4.5) at a dose of 55 mg/kg body weight on 5 consecutive days (to animals fasted for 6 hours) to induce diabetes.

Article Title: α-Linolenic acid but not linolenic acid protects against hypertension: critical role of SIRT3 and autophagic flux
Article Snippet: .. SIRT3 knock-out (SIRT3KO) and wild-type (WT) mice were obtained from Jackson Laboratory (Bar Harbor, Maine, USA), and hypertension was also induced by AngII infusion (0.4 mg/kg/d, 2 weeks). ..

Mouse Assay:

Article Title: IκB-kinase-ε in the tumor microenvironment is essential for the progression of gastric cancer
Article Snippet: .. Assessment of melanoma lung metastasis After confluence of culture in ordinary DMEM, B16-F10 were delivered to IKKε null mice and wild-type (WT) mice (purchased from The Jackson Laboratory) by tail-vein injection (2×105 cells/mouse). ..

Article Title: MOLECULAR MECHANISM OF THE ASSOCIATION BETWEEN ATRIAL FIBRILLATION AND HEART FAILURE INCLUDES ENERGY METABOLIC DYSREGULATION
Article Snippet: .. Cardiac specific liver kinase B1 (LKB1) knockout (KO) mice ( C57BL/6 ) were generated by crossing LKB1 flox/flox mice with transgenic mice expressing Cre-recombinase from the myosin heavy chain promoter., , LKB1 KO mice were born in SR and then developed spontaneous AF which followed with HF in persAF as we and others reported previously., , Wild-type (WT) mice were of the same strain as the corresponding transgenic mice (Jackson Lab). ..

Article Title: Endothelial exosome plays functional role during rickettsial infection
Article Snippet: .. Wild-type (WT) mice (C57BL/6J) were obtained from Jackson Laboratory (Bar Harbor, ME). .. C57BL/6J mice are highly susceptible to R. australis .

Article Title: The Absence of Indoleamine 2,3-Dioxygenase Inhibits Retinal Capillary Degeneration in Diabetic Mice
Article Snippet: .. IDO knockout (IDO−/− ) and wild-type (WT) mice (all on C57BL/6J background) were obtained from Jackson Laboratories (Bar Harbor, ME, USA). .. Male IDO−/− and WT mice at 3 months of age were administered five sequential intraperitoneal injections of streptozotocin (MP Biomedicals, Solon, OH, USA) solution freshly prepared in citrate buffer (pH 4.5) at a dose of 55 mg/kg body weight on 5 consecutive days (to animals fasted for 6 hours) to induce diabetes.

Article Title: α-Linolenic acid but not linolenic acid protects against hypertension: critical role of SIRT3 and autophagic flux
Article Snippet: .. SIRT3 knock-out (SIRT3KO) and wild-type (WT) mice were obtained from Jackson Laboratory (Bar Harbor, Maine, USA), and hypertension was also induced by AngII infusion (0.4 mg/kg/d, 2 weeks). ..

Article Title: The volatile anesthetic sevoflurane reduces neutrophil apoptosis via Fas death domain–Fas-associated death domain interaction
Article Snippet: .. Wild-type (WT) mice on the C57BL/6 background were purchased from The Jackson Laboratory (Bar Harbor, ME, USA) and inbred in our animal facility. ..

Article Title: Activation of TLR4 is necessary for trauma hemorrhagic shock-induced gut injury and PMN priming
Article Snippet: .. Male 10-12 week old outbred cesarean-derived (CD-1) mice, TLR4-mutated (C3H/HeJ) mice and their wild-type (WT) mice (C3H/HeOuJ), TRIF deficient and their wild type (C57BL/6J) littermates were obtained from The Jackson Laboratory. .. Mice on the C57BL/6J background with a specific deletion of the MyD88 gene (MyD88-/- mice) were kindly provided by Dr. Samuel J. Leibovich (UMDNJ-New Jersey Medical School, Newark, N.J).

Article Title: TREM-1 Attenuates RIPK3-mediated Necroptosis in Hyperoxia-induced Lung Injury in Neonatal Mice
Article Snippet: .. All breeding pairs of the wild-type (WT) laboratory mice of the C57BL/6J strain were purchased from The Jackson Laboratory, and breeding pairs of mice with targeted deletion of TREM-1/3 and RIPK3 genes on a C57BL/6J background were obtained from Genentech. ..

Transgenic Assay:

Article Title: MOLECULAR MECHANISM OF THE ASSOCIATION BETWEEN ATRIAL FIBRILLATION AND HEART FAILURE INCLUDES ENERGY METABOLIC DYSREGULATION
Article Snippet: .. Cardiac specific liver kinase B1 (LKB1) knockout (KO) mice ( C57BL/6 ) were generated by crossing LKB1 flox/flox mice with transgenic mice expressing Cre-recombinase from the myosin heavy chain promoter., , LKB1 KO mice were born in SR and then developed spontaneous AF which followed with HF in persAF as we and others reported previously., , Wild-type (WT) mice were of the same strain as the corresponding transgenic mice (Jackson Lab). ..

Generated:

Article Title: MOLECULAR MECHANISM OF THE ASSOCIATION BETWEEN ATRIAL FIBRILLATION AND HEART FAILURE INCLUDES ENERGY METABOLIC DYSREGULATION
Article Snippet: .. Cardiac specific liver kinase B1 (LKB1) knockout (KO) mice ( C57BL/6 ) were generated by crossing LKB1 flox/flox mice with transgenic mice expressing Cre-recombinase from the myosin heavy chain promoter., , LKB1 KO mice were born in SR and then developed spontaneous AF which followed with HF in persAF as we and others reported previously., , Wild-type (WT) mice were of the same strain as the corresponding transgenic mice (Jackson Lab). ..

Expressing:

Article Title: MOLECULAR MECHANISM OF THE ASSOCIATION BETWEEN ATRIAL FIBRILLATION AND HEART FAILURE INCLUDES ENERGY METABOLIC DYSREGULATION
Article Snippet: .. Cardiac specific liver kinase B1 (LKB1) knockout (KO) mice ( C57BL/6 ) were generated by crossing LKB1 flox/flox mice with transgenic mice expressing Cre-recombinase from the myosin heavy chain promoter., , LKB1 KO mice were born in SR and then developed spontaneous AF which followed with HF in persAF as we and others reported previously., , Wild-type (WT) mice were of the same strain as the corresponding transgenic mice (Jackson Lab). ..

Injection:

Article Title: IκB-kinase-ε in the tumor microenvironment is essential for the progression of gastric cancer
Article Snippet: .. Assessment of melanoma lung metastasis After confluence of culture in ordinary DMEM, B16-F10 were delivered to IKKε null mice and wild-type (WT) mice (purchased from The Jackson Laboratory) by tail-vein injection (2×105 cells/mouse). ..

Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 91
    The Jackson Laboratory tcrδ knockout mice wild type wt c57bl 6
    IgA and IgG2b levels are elevated in <t>TCRδ</t> −/− mice. Levels of Ig isotypes were determined by ELISA in serum (A), fecal pellet (B), and peritoneal lavage (C) from WT <t>(C57BL/6)</t> and TCRδ −/− mice. Data are expressed as means±standard error of the mean (n=3 mice). n.s., not significant. * p
    Tcrδ Knockout Mice Wild Type Wt C57bl 6, supplied by The Jackson Laboratory, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/tcrδ knockout mice wild type wt c57bl 6/product/The Jackson Laboratory
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    tcrδ knockout mice wild type wt c57bl 6 - by Bioz Stars, 2021-01
    91/100 stars
      Buy from Supplier

    85
    The Jackson Laboratory pathogen free male inbred wild type wt mice balb c
    Verification of cDC or pDC depletion by flow cytometry . Lung mononuclear cells were stained for DC subset markers. Cells are reported as percent of total population. Macrophages were excluded using FL1 autofluorescence and the macrophage specific marker F4/80. A) Myeloid dendritic cells: B220 - , Gr1 - , CD11b + and CD11c + . Wt <t>BALB/c</t> + DT (non-depleted control) vs. DTR Tg BALB/c + DT (depleted) yield a 63% depletion. B) Plasmacytoid dendritic cells: CD11clow, B220 + , and PDCA + . Wt + isotype Ab (non-depleted control) vs. Wt Balb/c + mPDCA-1 Ab (depleted) yields a 84% depletion. Data are representative of four to six mice in each group.
    Pathogen Free Male Inbred Wild Type Wt Mice Balb C, supplied by The Jackson Laboratory, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pathogen free male inbred wild type wt mice balb c/product/The Jackson Laboratory
    Average 85 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    pathogen free male inbred wild type wt mice balb c - by Bioz Stars, 2021-01
    85/100 stars
      Buy from Supplier

    85
    The Jackson Laboratory animals wild type wt mice
    (I) Effect of donor concentration and temperature on the uptake of 125 I-Aβ40 in <t>wild</t> <t>type</t> <t>(WT)</t> <t>mouse</t> brain slices. (II) Effect of endocytotic inhibitor dansyl cadaverine on the uptake of 125 I-Aβ40 (450 ng/ml) in WT mouse brain slices. (III) Histograms of fluorescence intensity in differentiated PC12 cells exposed to various concentrations of F-Aβ40. (A) Untreated cells; (B) Cells incubated with 0.65 µM F-Aβ40; (C) Cells incubated with 1.3 µM F-Aβ40; (D) Cells incubated with 3.2 µM F-Aβ40; (E) Cells incubated with 3.2 µM F-Aβ40+32 µM unlabeled Aβ40.
    Animals Wild Type Wt Mice, supplied by The Jackson Laboratory, used in various techniques. Bioz Stars score: 85/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/animals wild type wt mice/product/The Jackson Laboratory
    Average 85 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    animals wild type wt mice - by Bioz Stars, 2021-01
    85/100 stars
      Buy from Supplier

    91
    The Jackson Laboratory background snj wild type wt mice
    In vitro analysis of proliferation kinetics and myogenic differentiation of murine Dystrophin Expressing Chimeric Cells (DEC). a The DEC proliferation kinetics after fusion compared with <t>snj</t> wild type myoblasts (MB wt ) and dystrophin deficient <t>mdx</t> (MB mdx ) parent cells proliferation up to 21 days of culturing. Absolute cell counts (n = 3/cell type) at each time point (day 0, 3, 6, 9, 12, 15, 18, 21) were normalized with number of seeded cell and proliferation was expressed in fold increase. MB wt /MB mdx DEC cell proliferation results did not show differences in the maximal proliferation counts after fusion when compared to parent myoblast populations (p > 0.05, one-way ANOVA, not significant), confirming maintenance of efficient cell cycle with maximal proliferation peak reached 3 days earlier compared to not-fused controls. b Representative immunofluorescence images of DEC differentiated into skeletal myocytes expressing skeletal myosin heavy chain marker (SMHC-AlexaFluor 647, yellow) seven days after fusion. Confirmation of differentiation of MB wt /MB mdx DEC line to the skeletal myocytes in myogenic differentiation media comparable with MB wt controls. For merge: Yellow, SMHC; blue, DAPI (nuclei), scale bar 10 μm
    Background Snj Wild Type Wt Mice, supplied by The Jackson Laboratory, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/background snj wild type wt mice/product/The Jackson Laboratory
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    background snj wild type wt mice - by Bioz Stars, 2021-01
    91/100 stars
      Buy from Supplier

    Image Search Results


    IgA and IgG2b levels are elevated in TCRδ −/− mice. Levels of Ig isotypes were determined by ELISA in serum (A), fecal pellet (B), and peritoneal lavage (C) from WT (C57BL/6) and TCRδ −/− mice. Data are expressed as means±standard error of the mean (n=3 mice). n.s., not significant. * p

    Journal: Immune Network

    Article Title: Murine γδ T Cells Render B Cells Refractory to Commitment of IgA Isotype Switching

    doi: 10.4110/in.2018.18.e25

    Figure Lengend Snippet: IgA and IgG2b levels are elevated in TCRδ −/− mice. Levels of Ig isotypes were determined by ELISA in serum (A), fecal pellet (B), and peritoneal lavage (C) from WT (C57BL/6) and TCRδ −/− mice. Data are expressed as means±standard error of the mean (n=3 mice). n.s., not significant. * p

    Article Snippet: Animals and genotyping of TCRδ knockout mice Wild-type (WT) C57BL/6 (Daehan Biolink, Seoul, Korea) and TCRδ−/− mice ( ) (JAX stock #002119, Jackson Lab) were maintained on an 8:16-h light:dark cycle in an animal environmental control chamber (Daehan Biolink).

    Techniques: Mouse Assay, Enzyme-linked Immunosorbent Assay

    Verification of cDC or pDC depletion by flow cytometry . Lung mononuclear cells were stained for DC subset markers. Cells are reported as percent of total population. Macrophages were excluded using FL1 autofluorescence and the macrophage specific marker F4/80. A) Myeloid dendritic cells: B220 - , Gr1 - , CD11b + and CD11c + . Wt BALB/c + DT (non-depleted control) vs. DTR Tg BALB/c + DT (depleted) yield a 63% depletion. B) Plasmacytoid dendritic cells: CD11clow, B220 + , and PDCA + . Wt + isotype Ab (non-depleted control) vs. Wt Balb/c + mPDCA-1 Ab (depleted) yields a 84% depletion. Data are representative of four to six mice in each group.

    Journal: Respiratory Research

    Article Title: Donor lung derived myeloid and plasmacytoid dendritic cells differentially regulate T cell proliferation and cytokine production

    doi: 10.1186/1465-9921-13-25

    Figure Lengend Snippet: Verification of cDC or pDC depletion by flow cytometry . Lung mononuclear cells were stained for DC subset markers. Cells are reported as percent of total population. Macrophages were excluded using FL1 autofluorescence and the macrophage specific marker F4/80. A) Myeloid dendritic cells: B220 - , Gr1 - , CD11b + and CD11c + . Wt BALB/c + DT (non-depleted control) vs. DTR Tg BALB/c + DT (depleted) yield a 63% depletion. B) Plasmacytoid dendritic cells: CD11clow, B220 + , and PDCA + . Wt + isotype Ab (non-depleted control) vs. Wt Balb/c + mPDCA-1 Ab (depleted) yields a 84% depletion. Data are representative of four to six mice in each group.

    Article Snippet: Animals Specific pathogen-free male inbred wild-type (Wt) mice BALB/c (H2d ) and C57BL/6 (H2b ) were purchased from Harlan Sprague-Dawley (Indianapolis, IN) C.FVB-Tg(Itgax-DTR/EGFP)57Lan/J (CD11c-DTR) mice breeder pairs were purchased from The Jackson Laboratory (Bar Harbor, ME).

    Techniques: Flow Cytometry, Cytometry, Staining, Marker, Mouse Assay

    (I) Effect of donor concentration and temperature on the uptake of 125 I-Aβ40 in wild type (WT) mouse brain slices. (II) Effect of endocytotic inhibitor dansyl cadaverine on the uptake of 125 I-Aβ40 (450 ng/ml) in WT mouse brain slices. (III) Histograms of fluorescence intensity in differentiated PC12 cells exposed to various concentrations of F-Aβ40. (A) Untreated cells; (B) Cells incubated with 0.65 µM F-Aβ40; (C) Cells incubated with 1.3 µM F-Aβ40; (D) Cells incubated with 3.2 µM F-Aβ40; (E) Cells incubated with 3.2 µM F-Aβ40+32 µM unlabeled Aβ40.

    Journal: PLoS ONE

    Article Title: Mechanism of Neuronal versus Endothelial Cell Uptake of Alzheimer's Disease Amyloid ? Protein

    doi: 10.1371/journal.pone.0004627

    Figure Lengend Snippet: (I) Effect of donor concentration and temperature on the uptake of 125 I-Aβ40 in wild type (WT) mouse brain slices. (II) Effect of endocytotic inhibitor dansyl cadaverine on the uptake of 125 I-Aβ40 (450 ng/ml) in WT mouse brain slices. (III) Histograms of fluorescence intensity in differentiated PC12 cells exposed to various concentrations of F-Aβ40. (A) Untreated cells; (B) Cells incubated with 0.65 µM F-Aβ40; (C) Cells incubated with 1.3 µM F-Aβ40; (D) Cells incubated with 3.2 µM F-Aβ40; (E) Cells incubated with 3.2 µM F-Aβ40+32 µM unlabeled Aβ40.

    Article Snippet: Animals Wild type (WT) mice (B6/SJL) were obtained from The Jackson Laboratory (Bar Harbor, ME) at 6–8 weeks of age.

    Techniques: Concentration Assay, Fluorescence, Incubation

    In vitro analysis of proliferation kinetics and myogenic differentiation of murine Dystrophin Expressing Chimeric Cells (DEC). a The DEC proliferation kinetics after fusion compared with snj wild type myoblasts (MB wt ) and dystrophin deficient mdx (MB mdx ) parent cells proliferation up to 21 days of culturing. Absolute cell counts (n = 3/cell type) at each time point (day 0, 3, 6, 9, 12, 15, 18, 21) were normalized with number of seeded cell and proliferation was expressed in fold increase. MB wt /MB mdx DEC cell proliferation results did not show differences in the maximal proliferation counts after fusion when compared to parent myoblast populations (p > 0.05, one-way ANOVA, not significant), confirming maintenance of efficient cell cycle with maximal proliferation peak reached 3 days earlier compared to not-fused controls. b Representative immunofluorescence images of DEC differentiated into skeletal myocytes expressing skeletal myosin heavy chain marker (SMHC-AlexaFluor 647, yellow) seven days after fusion. Confirmation of differentiation of MB wt /MB mdx DEC line to the skeletal myocytes in myogenic differentiation media comparable with MB wt controls. For merge: Yellow, SMHC; blue, DAPI (nuclei), scale bar 10 μm

    Journal: Stem Cell Reviews

    Article Title: Creation of Dystrophin Expressing Chimeric Cells of Myoblast Origin as a Novel Stem Cell Based Therapy for Duchenne Muscular Dystrophy

    doi: 10.1007/s12015-017-9792-7

    Figure Lengend Snippet: In vitro analysis of proliferation kinetics and myogenic differentiation of murine Dystrophin Expressing Chimeric Cells (DEC). a The DEC proliferation kinetics after fusion compared with snj wild type myoblasts (MB wt ) and dystrophin deficient mdx (MB mdx ) parent cells proliferation up to 21 days of culturing. Absolute cell counts (n = 3/cell type) at each time point (day 0, 3, 6, 9, 12, 15, 18, 21) were normalized with number of seeded cell and proliferation was expressed in fold increase. MB wt /MB mdx DEC cell proliferation results did not show differences in the maximal proliferation counts after fusion when compared to parent myoblast populations (p > 0.05, one-way ANOVA, not significant), confirming maintenance of efficient cell cycle with maximal proliferation peak reached 3 days earlier compared to not-fused controls. b Representative immunofluorescence images of DEC differentiated into skeletal myocytes expressing skeletal myosin heavy chain marker (SMHC-AlexaFluor 647, yellow) seven days after fusion. Confirmation of differentiation of MB wt /MB mdx DEC line to the skeletal myocytes in myogenic differentiation media comparable with MB wt controls. For merge: Yellow, SMHC; blue, DAPI (nuclei), scale bar 10 μm

    Article Snippet: Six to eight -week old mice - mdx (C57BL/10ScSn-Dmdmdx/J, stock number 001801) with the respective background snj wild type (wt ) mice (C57BL/10ScSnJ, stock number 000476) were purchased from Jackson Laboratories.

    Techniques: In Vitro, Expressing, Immunofluorescence, Marker

    Significant increase of dystrophin expression at 30 days after DEC transplant to the gastrocnemius muscle (GM) of mdx mice. a Representative immunofluorescence images of dystrophin expression in GM of snj wild type ( wt ) mice (left, positive control), dystrophin-deficient mdx mice injected with vehicle, not fused MB wt with MB mdx and MB wt /MB mdx DEC. Restoration of dystrophin expression (magenta) is confirmed in GM of mdx mice injected with DEC. For merge: Magenta, dystrophin; blue, DAPI (nuclei), scale bar 10 μm. b Quantification of dystrophin-positive fibers at 30 days post-transplant confirms an increase of 37.27% in DEC injected mdx host compared to vehicle and not-fused MB wt and MB mdx controls; (n = 6, mean ± SD, 5 ROI/3 sections/6 animal/group, One-way ANOVA)

    Journal: Stem Cell Reviews

    Article Title: Creation of Dystrophin Expressing Chimeric Cells of Myoblast Origin as a Novel Stem Cell Based Therapy for Duchenne Muscular Dystrophy

    doi: 10.1007/s12015-017-9792-7

    Figure Lengend Snippet: Significant increase of dystrophin expression at 30 days after DEC transplant to the gastrocnemius muscle (GM) of mdx mice. a Representative immunofluorescence images of dystrophin expression in GM of snj wild type ( wt ) mice (left, positive control), dystrophin-deficient mdx mice injected with vehicle, not fused MB wt with MB mdx and MB wt /MB mdx DEC. Restoration of dystrophin expression (magenta) is confirmed in GM of mdx mice injected with DEC. For merge: Magenta, dystrophin; blue, DAPI (nuclei), scale bar 10 μm. b Quantification of dystrophin-positive fibers at 30 days post-transplant confirms an increase of 37.27% in DEC injected mdx host compared to vehicle and not-fused MB wt and MB mdx controls; (n = 6, mean ± SD, 5 ROI/3 sections/6 animal/group, One-way ANOVA)

    Article Snippet: Six to eight -week old mice - mdx (C57BL/10ScSn-Dmdmdx/J, stock number 001801) with the respective background snj wild type (wt ) mice (C57BL/10ScSnJ, stock number 000476) were purchased from Jackson Laboratories.

    Techniques: Expressing, Mouse Assay, Immunofluorescence, Positive Control, Injection

    Confirmation of ex vivo creation of murine Dystrophin Expressing Chimeric Cell (DEC) derived from the wild type snj myoblasts (MB wt ) and dystrophin-deficient mdx (MB mdx ) mice and confirmation of dystrophin expression by DECs after fusion. a Diagram of ex vivo polyethylene glycol (PEG) mediated cell fusion procedure to create DEC. b Flow cytometry plots presenting gating strategy used for DEC analysis; forward (FSC) vs. side (SSC) scatter to remove the signal of cell debris (left plot) and height vs. width side scatter to eliminate cell aggregates (right plot). c Representative flow cytometry plots of fusion of the PKH26-labeled MB wt and PKH67-labeled MB mdx parent myoblasts assessed by FACS. The overlapping fluorescence of PKH26/PKH67 confirms chimeric state for MB wt /MB mdx DEC cell line (far right). d Representative immunofluorescence images of dystrophin (magenta) in murine dystrophin-expressing MB wt , dystrophin-deficient MB mdx and MB wt /MB mdx DEC in vitro at 21 days after fusion confirming maintenance of dystrophin expression by DECs (n = 4, magnification 400X, scale bar 10 µm)

    Journal: Stem Cell Reviews

    Article Title: Creation of Dystrophin Expressing Chimeric Cells of Myoblast Origin as a Novel Stem Cell Based Therapy for Duchenne Muscular Dystrophy

    doi: 10.1007/s12015-017-9792-7

    Figure Lengend Snippet: Confirmation of ex vivo creation of murine Dystrophin Expressing Chimeric Cell (DEC) derived from the wild type snj myoblasts (MB wt ) and dystrophin-deficient mdx (MB mdx ) mice and confirmation of dystrophin expression by DECs after fusion. a Diagram of ex vivo polyethylene glycol (PEG) mediated cell fusion procedure to create DEC. b Flow cytometry plots presenting gating strategy used for DEC analysis; forward (FSC) vs. side (SSC) scatter to remove the signal of cell debris (left plot) and height vs. width side scatter to eliminate cell aggregates (right plot). c Representative flow cytometry plots of fusion of the PKH26-labeled MB wt and PKH67-labeled MB mdx parent myoblasts assessed by FACS. The overlapping fluorescence of PKH26/PKH67 confirms chimeric state for MB wt /MB mdx DEC cell line (far right). d Representative immunofluorescence images of dystrophin (magenta) in murine dystrophin-expressing MB wt , dystrophin-deficient MB mdx and MB wt /MB mdx DEC in vitro at 21 days after fusion confirming maintenance of dystrophin expression by DECs (n = 4, magnification 400X, scale bar 10 µm)

    Article Snippet: Six to eight -week old mice - mdx (C57BL/10ScSn-Dmdmdx/J, stock number 001801) with the respective background snj wild type (wt ) mice (C57BL/10ScSnJ, stock number 000476) were purchased from Jackson Laboratories.

    Techniques: Ex Vivo, Expressing, Derivative Assay, Mouse Assay, Flow Cytometry, Cytometry, Labeling, FACS, Fluorescence, Immunofluorescence, In Vitro