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rat albumin enzyme linked immunosorbent assay elisa quantitation kit  (Bethyl)


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    Bethyl rat albumin enzyme linked immunosorbent assay elisa quantitation kit
    Figure 8. Loss of MC1R potentiates B-cell activation and en- hances autologous humoral immune responses in rats with PHN. (A) Animals were treated as elaborated in Figure 1F. Splenocytes derived from WT or KO rats with PHN were pro- cessed for flow cytometry analysis of CD1381 cells. (B) Arbitrary levels of sheep IgG-specific rat IgG in sera collected from WT or KO rats with PHN, as estimated by <t>ELISA</t> of diluted sera; aP,0.05 versus WT rats with PHN (n56). (C) Schematic diagram depicting the working model for negative regulation of B-cell activation by MC1R-mediated melanocortinergic signaling. As a typical G-protein coupled receptor, MC1R is expressed by B lympho- cytes and is able to trigger the cAMP signaling pathway on ac- tivation by diverse melanocortins, such as pan-MCR agonists like ACTH and NDP-MSH, or the selective MC1R agonist MS05. Subsequently, cAMP signaling downstream of MC1R activates MITF, one of the major signaling transducers of MC1R pathway and a critical regulator of a plethora of key cellular processes, including melanogenesis in melanocytes and cellular differenti- ation in nonmelanocytic cells. In B lymphocytes, MITF acts as a repressor of IRF4, a characteristic lymphoid transcription factor essential for B-cell development and maturation. MC1R-medi- ated melanocortinergic signaling suppresses B-cell activation and plasmacytic differentiation and reduces IgG production via the cAMP/MITF/IRF4 pathway, which could be intercepted by SQ22536, an adenylyl cyclase inhibitor. This MC1R-mediated B- cell regulatory signaling is defective in B cells with MC1R KO and could be partially restored by the cAMP mimetic dBcAMP.
    Rat Albumin Enzyme Linked Immunosorbent Assay Elisa Quantitation Kit, supplied by Bethyl, used in various techniques. Bioz Stars score: 94/100, based on 320 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rat albumin enzyme linked immunosorbent assay elisa quantitation kit/product/Bethyl
    Average 94 stars, based on 320 article reviews
    rat albumin enzyme linked immunosorbent assay elisa quantitation kit - by Bioz Stars, 2026-02
    94/100 stars

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    1) Product Images from "Negative Modulation of B Cell Activation by Melanocortin 1 Receptor Signaling Protects against Membranous Nephropathy"

    Article Title: Negative Modulation of B Cell Activation by Melanocortin 1 Receptor Signaling Protects against Membranous Nephropathy

    Journal: Journal of the American Society of Nephrology

    doi: 10.1681/asn.2022050605

    Figure 8. Loss of MC1R potentiates B-cell activation and en- hances autologous humoral immune responses in rats with PHN. (A) Animals were treated as elaborated in Figure 1F. Splenocytes derived from WT or KO rats with PHN were pro- cessed for flow cytometry analysis of CD1381 cells. (B) Arbitrary levels of sheep IgG-specific rat IgG in sera collected from WT or KO rats with PHN, as estimated by ELISA of diluted sera; aP,0.05 versus WT rats with PHN (n56). (C) Schematic diagram depicting the working model for negative regulation of B-cell activation by MC1R-mediated melanocortinergic signaling. As a typical G-protein coupled receptor, MC1R is expressed by B lympho- cytes and is able to trigger the cAMP signaling pathway on ac- tivation by diverse melanocortins, such as pan-MCR agonists like ACTH and NDP-MSH, or the selective MC1R agonist MS05. Subsequently, cAMP signaling downstream of MC1R activates MITF, one of the major signaling transducers of MC1R pathway and a critical regulator of a plethora of key cellular processes, including melanogenesis in melanocytes and cellular differenti- ation in nonmelanocytic cells. In B lymphocytes, MITF acts as a repressor of IRF4, a characteristic lymphoid transcription factor essential for B-cell development and maturation. MC1R-medi- ated melanocortinergic signaling suppresses B-cell activation and plasmacytic differentiation and reduces IgG production via the cAMP/MITF/IRF4 pathway, which could be intercepted by SQ22536, an adenylyl cyclase inhibitor. This MC1R-mediated B- cell regulatory signaling is defective in B cells with MC1R KO and could be partially restored by the cAMP mimetic dBcAMP.
    Figure Legend Snippet: Figure 8. Loss of MC1R potentiates B-cell activation and en- hances autologous humoral immune responses in rats with PHN. (A) Animals were treated as elaborated in Figure 1F. Splenocytes derived from WT or KO rats with PHN were pro- cessed for flow cytometry analysis of CD1381 cells. (B) Arbitrary levels of sheep IgG-specific rat IgG in sera collected from WT or KO rats with PHN, as estimated by ELISA of diluted sera; aP,0.05 versus WT rats with PHN (n56). (C) Schematic diagram depicting the working model for negative regulation of B-cell activation by MC1R-mediated melanocortinergic signaling. As a typical G-protein coupled receptor, MC1R is expressed by B lympho- cytes and is able to trigger the cAMP signaling pathway on ac- tivation by diverse melanocortins, such as pan-MCR agonists like ACTH and NDP-MSH, or the selective MC1R agonist MS05. Subsequently, cAMP signaling downstream of MC1R activates MITF, one of the major signaling transducers of MC1R pathway and a critical regulator of a plethora of key cellular processes, including melanogenesis in melanocytes and cellular differenti- ation in nonmelanocytic cells. In B lymphocytes, MITF acts as a repressor of IRF4, a characteristic lymphoid transcription factor essential for B-cell development and maturation. MC1R-medi- ated melanocortinergic signaling suppresses B-cell activation and plasmacytic differentiation and reduces IgG production via the cAMP/MITF/IRF4 pathway, which could be intercepted by SQ22536, an adenylyl cyclase inhibitor. This MC1R-mediated B- cell regulatory signaling is defective in B cells with MC1R KO and could be partially restored by the cAMP mimetic dBcAMP.

    Techniques Used: Activation Assay, Derivative Assay, Cytometry, Enzyme-linked Immunosorbent Assay



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    Figure 8. Loss of MC1R potentiates B-cell activation and en- hances autologous humoral immune responses in rats with PHN. (A) Animals were treated as elaborated in Figure 1F. Splenocytes derived from WT or KO rats with PHN were pro- cessed for flow cytometry analysis of CD1381 cells. (B) Arbitrary levels of sheep IgG-specific rat IgG in sera collected from WT or KO rats with PHN, as estimated by <t>ELISA</t> of diluted sera; aP,0.05 versus WT rats with PHN (n56). (C) Schematic diagram depicting the working model for negative regulation of B-cell activation by MC1R-mediated melanocortinergic signaling. As a typical G-protein coupled receptor, MC1R is expressed by B lympho- cytes and is able to trigger the cAMP signaling pathway on ac- tivation by diverse melanocortins, such as pan-MCR agonists like ACTH and NDP-MSH, or the selective MC1R agonist MS05. Subsequently, cAMP signaling downstream of MC1R activates MITF, one of the major signaling transducers of MC1R pathway and a critical regulator of a plethora of key cellular processes, including melanogenesis in melanocytes and cellular differenti- ation in nonmelanocytic cells. In B lymphocytes, MITF acts as a repressor of IRF4, a characteristic lymphoid transcription factor essential for B-cell development and maturation. MC1R-medi- ated melanocortinergic signaling suppresses B-cell activation and plasmacytic differentiation and reduces IgG production via the cAMP/MITF/IRF4 pathway, which could be intercepted by SQ22536, an adenylyl cyclase inhibitor. This MC1R-mediated B- cell regulatory signaling is defective in B cells with MC1R KO and could be partially restored by the cAMP mimetic dBcAMP.
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    Figure 8. Loss of MC1R potentiates B-cell activation and en- hances autologous humoral immune responses in rats with PHN. (A) Animals were treated as elaborated in Figure 1F. Splenocytes derived from WT or KO rats with PHN were pro- cessed for flow cytometry analysis of CD1381 cells. (B) Arbitrary levels of sheep IgG-specific rat IgG in sera collected from WT or KO rats with PHN, as estimated by <t>ELISA</t> of diluted sera; aP,0.05 versus WT rats with PHN (n56). (C) Schematic diagram depicting the working model for negative regulation of B-cell activation by MC1R-mediated melanocortinergic signaling. As a typical G-protein coupled receptor, MC1R is expressed by B lympho- cytes and is able to trigger the cAMP signaling pathway on ac- tivation by diverse melanocortins, such as pan-MCR agonists like ACTH and NDP-MSH, or the selective MC1R agonist MS05. Subsequently, cAMP signaling downstream of MC1R activates MITF, one of the major signaling transducers of MC1R pathway and a critical regulator of a plethora of key cellular processes, including melanogenesis in melanocytes and cellular differenti- ation in nonmelanocytic cells. In B lymphocytes, MITF acts as a repressor of IRF4, a characteristic lymphoid transcription factor essential for B-cell development and maturation. MC1R-medi- ated melanocortinergic signaling suppresses B-cell activation and plasmacytic differentiation and reduces IgG production via the cAMP/MITF/IRF4 pathway, which could be intercepted by SQ22536, an adenylyl cyclase inhibitor. This MC1R-mediated B- cell regulatory signaling is defective in B cells with MC1R KO and could be partially restored by the cAMP mimetic dBcAMP.
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    Figure 8. Loss of MC1R potentiates B-cell activation and en- hances autologous humoral immune responses in rats with PHN. (A) Animals were treated as elaborated in Figure 1F. Splenocytes derived from WT or KO rats with PHN were pro- cessed for flow cytometry analysis of CD1381 cells. (B) Arbitrary levels of sheep IgG-specific rat IgG in sera collected from WT or KO rats with PHN, as estimated by <t>ELISA</t> of diluted sera; aP,0.05 versus WT rats with PHN (n56). (C) Schematic diagram depicting the working model for negative regulation of B-cell activation by MC1R-mediated melanocortinergic signaling. As a typical G-protein coupled receptor, MC1R is expressed by B lympho- cytes and is able to trigger the cAMP signaling pathway on ac- tivation by diverse melanocortins, such as pan-MCR agonists like ACTH and NDP-MSH, or the selective MC1R agonist MS05. Subsequently, cAMP signaling downstream of MC1R activates MITF, one of the major signaling transducers of MC1R pathway and a critical regulator of a plethora of key cellular processes, including melanogenesis in melanocytes and cellular differenti- ation in nonmelanocytic cells. In B lymphocytes, MITF acts as a repressor of IRF4, a characteristic lymphoid transcription factor essential for B-cell development and maturation. MC1R-medi- ated melanocortinergic signaling suppresses B-cell activation and plasmacytic differentiation and reduces IgG production via the cAMP/MITF/IRF4 pathway, which could be intercepted by SQ22536, an adenylyl cyclase inhibitor. This MC1R-mediated B- cell regulatory signaling is defective in B cells with MC1R KO and could be partially restored by the cAMP mimetic dBcAMP.
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    rat albumin enzyme linked immunosorbent assay quantitation kit  (Bethyl)
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    Figure 8. Loss of MC1R potentiates B-cell activation and en- hances autologous humoral immune responses in rats with PHN. (A) Animals were treated as elaborated in Figure 1F. Splenocytes derived from WT or KO rats with PHN were pro- cessed for flow cytometry analysis of CD1381 cells. (B) Arbitrary levels of sheep IgG-specific rat IgG in sera collected from WT or KO rats with PHN, as estimated by <t>ELISA</t> of diluted sera; aP,0.05 versus WT rats with PHN (n56). (C) Schematic diagram depicting the working model for negative regulation of B-cell activation by MC1R-mediated melanocortinergic signaling. As a typical G-protein coupled receptor, MC1R is expressed by B lympho- cytes and is able to trigger the cAMP signaling pathway on ac- tivation by diverse melanocortins, such as pan-MCR agonists like ACTH and NDP-MSH, or the selective MC1R agonist MS05. Subsequently, cAMP signaling downstream of MC1R activates MITF, one of the major signaling transducers of MC1R pathway and a critical regulator of a plethora of key cellular processes, including melanogenesis in melanocytes and cellular differenti- ation in nonmelanocytic cells. In B lymphocytes, MITF acts as a repressor of IRF4, a characteristic lymphoid transcription factor essential for B-cell development and maturation. MC1R-medi- ated melanocortinergic signaling suppresses B-cell activation and plasmacytic differentiation and reduces IgG production via the cAMP/MITF/IRF4 pathway, which could be intercepted by SQ22536, an adenylyl cyclase inhibitor. This MC1R-mediated B- cell regulatory signaling is defective in B cells with MC1R KO and could be partially restored by the cAMP mimetic dBcAMP.
    Rat Albumin Enzyme Linked Immunosorbent Assay Quantitation Kit, supplied by Bethyl, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 1 article reviews
    rat albumin enzyme linked immunosorbent assay quantitation kit - by Bioz Stars, 2026-02
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    Figure 8. Loss of MC1R potentiates B-cell activation and en- hances autologous humoral immune responses in rats with PHN. (A) Animals were treated as elaborated in Figure 1F. Splenocytes derived from WT or KO rats with PHN were pro- cessed for flow cytometry analysis of CD1381 cells. (B) Arbitrary levels of sheep IgG-specific rat IgG in sera collected from WT or KO rats with PHN, as estimated by ELISA of diluted sera; aP,0.05 versus WT rats with PHN (n56). (C) Schematic diagram depicting the working model for negative regulation of B-cell activation by MC1R-mediated melanocortinergic signaling. As a typical G-protein coupled receptor, MC1R is expressed by B lympho- cytes and is able to trigger the cAMP signaling pathway on ac- tivation by diverse melanocortins, such as pan-MCR agonists like ACTH and NDP-MSH, or the selective MC1R agonist MS05. Subsequently, cAMP signaling downstream of MC1R activates MITF, one of the major signaling transducers of MC1R pathway and a critical regulator of a plethora of key cellular processes, including melanogenesis in melanocytes and cellular differenti- ation in nonmelanocytic cells. In B lymphocytes, MITF acts as a repressor of IRF4, a characteristic lymphoid transcription factor essential for B-cell development and maturation. MC1R-medi- ated melanocortinergic signaling suppresses B-cell activation and plasmacytic differentiation and reduces IgG production via the cAMP/MITF/IRF4 pathway, which could be intercepted by SQ22536, an adenylyl cyclase inhibitor. This MC1R-mediated B- cell regulatory signaling is defective in B cells with MC1R KO and could be partially restored by the cAMP mimetic dBcAMP.

    Journal: Journal of the American Society of Nephrology

    Article Title: Negative Modulation of B Cell Activation by Melanocortin 1 Receptor Signaling Protects against Membranous Nephropathy

    doi: 10.1681/asn.2022050605

    Figure Lengend Snippet: Figure 8. Loss of MC1R potentiates B-cell activation and en- hances autologous humoral immune responses in rats with PHN. (A) Animals were treated as elaborated in Figure 1F. Splenocytes derived from WT or KO rats with PHN were pro- cessed for flow cytometry analysis of CD1381 cells. (B) Arbitrary levels of sheep IgG-specific rat IgG in sera collected from WT or KO rats with PHN, as estimated by ELISA of diluted sera; aP,0.05 versus WT rats with PHN (n56). (C) Schematic diagram depicting the working model for negative regulation of B-cell activation by MC1R-mediated melanocortinergic signaling. As a typical G-protein coupled receptor, MC1R is expressed by B lympho- cytes and is able to trigger the cAMP signaling pathway on ac- tivation by diverse melanocortins, such as pan-MCR agonists like ACTH and NDP-MSH, or the selective MC1R agonist MS05. Subsequently, cAMP signaling downstream of MC1R activates MITF, one of the major signaling transducers of MC1R pathway and a critical regulator of a plethora of key cellular processes, including melanogenesis in melanocytes and cellular differenti- ation in nonmelanocytic cells. In B lymphocytes, MITF acts as a repressor of IRF4, a characteristic lymphoid transcription factor essential for B-cell development and maturation. MC1R-medi- ated melanocortinergic signaling suppresses B-cell activation and plasmacytic differentiation and reduces IgG production via the cAMP/MITF/IRF4 pathway, which could be intercepted by SQ22536, an adenylyl cyclase inhibitor. This MC1R-mediated B- cell regulatory signaling is defective in B cells with MC1R KO and could be partially restored by the cAMP mimetic dBcAMP.

    Article Snippet: Urinary albumin concentrations were analyzed using a rat albumin enzyme-linked immunosorbent assay (ELISA) quantitation kit (Bethyl Laboratories Inc., Montgomery, TX) or an albumin assay kit (BioAssay System, Hayward, CA).

    Techniques: Activation Assay, Derivative Assay, Cytometry, Enzyme-linked Immunosorbent Assay