Anti anp

Manufactured by Santa Cruz Biotechnology

Sourced in United States

Anti-ANP is a laboratory reagent used for the detection and quantification of Atrial Natriuretic Peptide (ANP) in biological samples. It is a specific antibody that binds to ANP, allowing for its identification and measurement.

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Lab products found in correlation

Anti nanog, by Abcam (2 mentions) Anti oct3 4, by Santa Cruz Biotechnology (2 mentions) Anti ssea 3, by Merck Group (2 mentions) Anti tra 1 81, by Merck Group (2 mentions) Anti bnp, by Santa Cruz Biotechnology (2 mentions) Anti akt, by Cell Signaling Technology (2 mentions) Bca protein assay kit, by Thermo Fisher Scientific (2 mentions) Bq123, by Merck Group (1 mentions) Angiotensin 2, by Merck Group (1 mentions) Endothelin 1, by Merck Group (1 mentions) Nfatc4, by Santa Cruz Biotechnology (1 mentions) Bq788, by Merck Group (1 mentions) Monoclonal anti α actinin, by Merck Group (1 mentions) Anti cmybp c, by Santa Cruz Biotechnology (1 mentions) Alexa fluor 488 chicken anti rabbit igg, by Thermo Fisher Scientific (1 mentions) Alexa fluor 594 goat anti mouse igg1, by Thermo Fisher Scientific (1 mentions) Goat anti rat igm alexa fluor 488, by Thermo Fisher Scientific (1 mentions) Goat anti mouse igg2b alexa fluor 594, by Thermo Fisher Scientific (1 mentions) Alexa fluor 594 goat anti mouse igm, by Thermo Fisher Scientific (1 mentions) Insulin like growth factor 1, by Merck Group (1 mentions)

8 protocols using anti anp

Immunofluorescence Staining of Pluripotency and Cardiac Markers

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Immunofluorescence staining for pluripotency of iPSCs was performed by using the following primary antibodies: anti‐NANOG (Abcam), anti‐OCT3/4 (Santa Cruz), anti–SSEA 3 (Millipore), anti–SSEA 4 (Millipore), anti–Tra‐1‐60 (Millipore), and anti–Tra‐1‐81 (Millipore). In immunofluorescence staining for cardiac markers, monoclonal anti–α‐actinin (Sigma), monoclonal anti‐cTnT (Thermo Scientific), polyclonal anti‐cTnT (Santa Cruz), monoclonal anti–myosin light chain (MLC)2a (Synaptic Systems), polyclonal anti‐MLC2v (ProteinTech Group), anti‐ANP (Santa Cruz), anti–cMyBP‐C (Santa Cruz), polyclonal anti–cMyBP‐C motif (supplied by C. Witt University of Heidelberg, Heidelberg, Germany), and anti–nuclear factor of activated T cells (NFAT)c4 (Santa Cruz) were used. The isotype‐specific secondary antibodies, Alexa Fluor 488 chicken anti‐rabbit IgG, Alexa Fluor 594 goat anti‐mouse IgG₁, Alexa Fluor 488 goat anti‐rat IgM, Alexa Fluor 594 goat anti‐mouse IgM, Alexa Fluor 488 goat anti‐mouse IgG, Alexa Fluor 594 goat anti‐mouse IgG_2b, Alexa Fluor 594 chicken anti‐goat IgG, and Alexa Fluor 555 goat anti‐rabbit IgG, were all obtained from Invitrogen. The tested drugs included endothelin‐1 (1.0, 10, 100, or 1000 nmol/L), angiotensin II (100 nmol/L), insulin‐like growth factor 1 (100 nmol/L), phenylephrine (0.05 mmol/L), BQ‐123 (250 nmol/L), and BQ‐788 (100 nmol/L) (all from Sigma).

Tanaka A., Yuasa S., Mearini G., Egashira T., Seki T., Kodaira M., Kusumoto D., Kuroda Y., Okata S., Suzuki T., Inohara T., Arimura T., Makino S., Kimura K., Kimura A., Furukawa T., Carrier L., Node K, & Fukuda K. (2014). Endothelin‐1 Induces Myofibrillar Disarray and Contractile Vector Variability in Hypertrophic Cardiomyopathy–Induced Pluripotent Stem Cell–Derived Cardiomyocytes. Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 3(6), e001263.

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Cardiac Histomorphometry and Hypertrophy Evaluation

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Animals were anesthetized using avertin (250 mg/kg i.p. injection). The chest was opened and an apical injection of 1 M KCl arrested the heart in diastole. Hearts were perfusion-fixed with 4% buffered formalin at physiological pressure, post-fixed in formalin, embedded in paraffin, sectioned at 6 μm, and stained with Masson's Trichrome or hematoxylin and eosin (H&E). Cardiac morphometry was performed with Aperio ImageScope Viewer software (Aperio Technologies) using digital planimetry [14,16] . Infarcted/scarred LV area was calculated as a % of total LV area. Cardiac hypertrophy was quantified as the heart weight-to or ventricular weight-to-body weight or tibia length ratio. LV atrial natriuretic peptide (ANP) expression was determined via immunohistochemistry utilizing anti-ANP (Santa Cruz) antibody.

Ussher J.R., Baggio L.L., Campbell J.E., Mulvihill E.E., Kim M., Kabir M.G., Cao X., Baranek B.M., Stoffers D.A., Seeley R.J, & Drucker D.J. (2014). Inactivation of the cardiomyocyte glucagon-like peptide-1 receptor (GLP-1R) unmasks cardiomyocyte-independent GLP-1R-mediated cardioprotection. Molecular Metabolism, 3(5), 507-517.

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Comprehensive Antibody Analysis in Cardiovascular Research

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The following antibodies were used in this study: anti-IGF-IIR (#ab124767, Abcam, Cambridge, UK), anti-HSF2 (#sc-13056, Santa Cruz, CA, USA), anti-p53 (#2524, Cell Signaling Technology, MA, USA), anti-phospho-p53 (#9284, Cell Signaling Technology, Danvers, MA, USA), anti-BNP (sc-18818, Santa Cruz), anti-ANP (sc-20158, Santa Cruz), anti-β-actin (sc-47778, Santa Cruz), anti-cTnI (ab19615, Abcam), anti-HDAC1, anti-GAPDH (sc-137179, Santa Cruz), anti-STAT3 (sc-483, Santa Cruz), anti-c-myc (sc-42, Santa Cruz), anti-Tubulin (sc-5286, Santa Cruz) and anti-phospho-cTnI (#4004, Cell Signaling Technology). All secondary antibodies (HRP-conjugated anti-rabbit, anti-mouse and anti-goat) were purchased from Santa Cruz Biotechnology. All reagents were purchased from Sigma.

Huang C.Y., Pai P.Y., Kuo C.H., Ho T.J., Lin J.Y., Lin D.Y., Tsai F.J., Padma V.V., Kuo W.W, & Huang C.Y. (2017). p53-mediated miR-18 repression activates HSF2 for IGF-IIR-dependent myocyte hypertrophy in hypertension-induced heart failure. Cell Death & Disease, 8(8), e2990-.

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Pluripotent Stem Cell Characterization

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Colonies of undifferentiated human iPSCs plated on MEF feeder cells and cardiomyocytes plated on fibronectin-coated dishes were fixed with 4% paraformaldehyde (MUTO Pure Chemicals, Tokyo, Japan) for 30 min at 4 °C. After fixation, cells were permeabilized with 1% Triton X-100 and blocked with ImmunoBlock (DS Pharma Biomedical, Osaka, Japan). Specimens were incubated at 4 °C overnight with each of the following primary antibodies: anti-OCT3/4 (Santa Cruz, CA, USA), anti-NANOG (Abcam, Camb, UK), anti-SSEA3 (Millipore, MA, USA), anti-Tra1-81 (Millipore), anti-TroponinT (Thermo Scientific, MA, USA), anti-alpha-actinin (Sigma-Aldrich), anti-GATA4 (Santa Cruz) and anti-ANP (Santa Cruz). Preparations were incubated with secondary antibodies for 1 h at room temperature. Nuclei were counterstained with 50 ng/ml 4′,6′-diamidino-2-phenylindole (DAPI; Invitrogen). Fluorescent signals were detected using a fluorescence laser microscope equipped with 1.5×10⁵ pixels charged coupled device (CCD) camera (BZ-9000, Keyence, Osaka, Japan).

Kuroda Y., Yuasa S., Watanabe Y., Ito S., Egashira T., Seki T., Hattori T., Ohno S., Kodaira M., Suzuki T., Hashimoto H., Okata S., Tanaka A., Aizawa Y., Murata M., Aiba T., Makita N., Furukawa T., Shimizu W., Kodama I., Ogawa S., Kokubun N., Horigome H., Horie M., Kamiya K, & Fukuda K. (2017). Flecainide ameliorates arrhythmogenicity through NCX flux in Andersen-Tawil syndrome-iPS cell-derived cardiomyocytes. Biochemistry and Biophysics Reports, 9, 245-256.

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Intercellular Signaling Analysis in Cardiomyocytes

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Whole protein from NRCMs or mouse heart tissue was extracted as previously reported 11 (link). Intercellular signaling was analyzed using a Pathscan Intercellular Signaling Array kit (#7323 and #12856; Cell Signaling Technology, Inc.) following the protocol provided, and routine western blotting procedures were performed according to our previous report 11 (link). The primary antibodies used were as follows: anti-ANP (mouse mAb; 1:300; sc-515701; Santa Cruz Biotechnology, Inc.), anti-BNP (rabbit pAb; 1:500; ab19645; Abcam), anti-MYH7 (mouse mAb; 1:300; sc-53089; Santa Cruz Biotechnology, Inc.), anti-Erk1/2 (rabbit mAb; 1:1000; #9102), anti-phospho-Erk1/2 (Thr202/Thr204) (rabbit mAb; 1:1000; #9102), anti-Akt (rabbit mAb; 1:1000; #9272), anti-phospho-Akt (Ser473) (rabbit mAb; 1:1000; #4060), anti-PKC (rabbit mAb; 1:1000; #2056), anti-phospho-PKC pan (Thr514) (rabbit mAb; 1:1000; #9379), anti-AMPK (rabbit mAb; 1:1000; #5831), anti-phospho-AMPK (Thr172) (rabbit mAb; 1:1000; #2535), and anti-GAPDH (rabbit mAb; 1:2000; #2118;Cell Signaling Technology, Inc.). The secondary antibodies used were horseradish peroxidase (HRP) conjugated (GE Healthcare Life Sciences, Beijing, China): anti-mouse IgG, HRP-conjugated whole Ab sheep (NA931) or anti-rabbit IgG, HRP-linked whole Ab donkey (NA934).

Weng X., Liu H., Zhang X., Sun Q., Li C., Gu M., Xu Y., Li S., Li W, & Du J. (2020). An α2-adrenoceptor agonist: Dexmedetomidine induces protective cardiomyocyte hypertrophy through mitochondrial-AMPK pathway. International Journal of Medical Sciences, 17(16), 2454-2467.

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Investigating Cellular Stress Responses

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The fetal bovine serum FBS and EDTA were obtained from Gibco (NY, USA). The 2′,7′-Dichlorofluorescein diacetate (DCFHDA), 5,58,6,68-tetraethylbenzimidazolcarbocyanine iodide (JC-1), doxorubicin (Dox), LY294002, ML 385, and glutathione (GSH) were bought from Sigma-Aldrich (St. Louis, MO, USA). The anti-AKT, anti-phospho-AKT, anti-β-actin, anti-Nrf2, anti-PCNA, anti-HO-1, anti-NQO1, and anti-NFkBp65 antibodies were obtained from Cell Signaling Technology (Danvers, MA, USA). The anti-BNP, anti-ANP, anti-Smad3, anti-phospho-Smad3, anti-p38, anti-phospho-p38, anti-α-SMA, anti-fibronectin, and anti-collagen 1 antibodies were obtained from Santa Cruz Biotechnology (Dallas, CA, USA). The secondary antibodies with HRP conjugated were bought from Sigma-Aldrich (St. Louis, MO, USA).

Hsieh P.L., Chu P.M., Cheng H.C., Huang Y.T., Chou W.C., Tsai K.L, & Chan S.H. (2022). Dapagliflozin Mitigates Doxorubicin-Caused Myocardium Damage by Regulating AKT-Mediated Oxidative Stress, Cardiac Remodeling, and Inflammation. International Journal of Molecular Sciences, 23(17), 10146.

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Western Blot Analysis of Cardiac Markers

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H9C2 cells were lysed in ice-cold lysis buffer and centrifuged at 12 000g at 4°C for 20 minutes. Total protein was separated by 10% SDS-PAGE and transferred onto polyvinylidene fluoride membranes (Merck KGaA, Darmstadt, Germany). After blocking with 5% nonfat milk for 3 hours, membranes were incubated overnight at 4°C with primary antibodies, including anti-IL-6, anti-IL-10, anti-BNP (B-type natriuretic peptide), anti-GAPDH (Abclone Biotechnology, Hurstbridge, Australia), and anti-ANP (Santa Cruz Biotechnology, Dallas, TX), followed by horseradish peroxidase-conjugated secondary antibodies. The bands were visualized with an enhanced chemiluminescence system (Thermo Fisher Scientific).

Zhou L., Miao K., Yin B., Li H., Fan J., Zhu Y., Ba H., Zhang Z., Chen F., Wang J., Zhao C., Li Z, & Wang D.W. (2018). Cardioprotective Role of Myeloid-Derived Suppressor Cells in Heart Failure. Circulation, 138(2).

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Cardiomyocyte Protein Expression Analysis

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Total protein was extracted from cultured neonatal cardiomyocytes and protein concentration was measured using a BCA protein assay kit (Thermo Scientific, USA). Protein samples were separated by 8% or 12% acrylamide denaturing gels (SDS-PAGE) and then transferred to polyvinylidene difluoride (PVDF) membranes. Following transfer, membranes were washed with tris-buffered saline and polysorbate 20 (TBST), and then blocked in 5% skim milk (Gibco, USA) in TBST for 2 h at room temperature, followed by incubation with anti-ANP (1:1000 dilution, Santa Cruz Biotechnology), anti-β-MHC (1:1000 dilution, Santa Cruz Biotechnology), anti-phospho-Smad3 antibody (p-Smad3, 1:1000 dilution, CST), anti-Smad3 antibody (1:1000 dilution, CST) and anti-GADPH (1:10,000 dilution, BOSTER) antibodies on a shaker overnight at 4 °C. The following day, membranes were washed in TBST and then incubated with secondary antibodies (1:8000 dilution, BOSTER) for 2 h at room temperature. Antibody-antigen complexes in all membranes were detected using the Imaging System (GE, Amersham Image 600) and protein bands were quantified by Image Pro Plus 6.0.

Li Z., Wu Z., Yan J., Liu H., Liu Q., Deng Y., Ou C, & Chen M. (2019). Gut microbe-derived metabolite trimethylamine N-oxide induces cardiac hypertrophy and fibrosis. Laboratory investigation; a journal of technical methods and pathology, 99(3).

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