l 6 rat specific elisa kit Search Results


nebnext ribosomal rna rrna depletion kit  (New England Biolabs)
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Nebnext Ribosomal Rna Rrna Depletion Kit, supplied by New England Biolabs, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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enzyme linked immunosorbent assay elisa kit  (Aviva Systems)
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Aviva Systems enzyme linked immunosorbent assay elisa kit
Enzyme Linked Immunosorbent Assay Elisa Kit, supplied by Aviva Systems, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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rat igg elisa kit  (Aviva Systems)
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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 <t>sheep</t> <t>IgG-specific</t> 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 Igg Elisa Kit, supplied by Aviva Systems, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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truseq stranded total rna human mouse rat kit  (Illumina Inc)
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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 <t>sheep</t> <t>IgG-specific</t> 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.
Truseq Stranded Total Rna Human Mouse Rat Kit, supplied by Illumina Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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truseq stranded total rna ht sample prep kit  (Illumina Inc)
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Illumina Inc truseq stranded total rna ht sample prep 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 <t>sheep</t> <t>IgG-specific</t> 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.
Truseq Stranded Total Rna Ht Sample Prep Kit, supplied by Illumina Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human mouse rat  (New England Biolabs)
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New England Biolabs human mouse rat
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 <t>sheep</t> <t>IgG-specific</t> 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.
Human Mouse Rat, supplied by New England Biolabs, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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rneasy mini kit  (Qiagen)
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Qiagen rneasy mini 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 <t>sheep</t> <t>IgG-specific</t> 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.
Rneasy Mini Kit, supplied by Qiagen, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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truseq stranded total rna library kit  (Illumina Inc)
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Illumina Inc truseq stranded total rna library 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 <t>sheep</t> <t>IgG-specific</t> 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.
Truseq Stranded Total Rna Library Kit, supplied by Illumina Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/l+6+rat+specific+elisa+kit/pm30791746-27-5-4?v=Illumina+Inc
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nebnext rrna depletion kit v2  (New England Biolabs)
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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 <t>sheep</t> <t>IgG-specific</t> 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.
Nebnext Rrna Depletion Kit V2, supplied by New England Biolabs, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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nebnext rrna depletion kit  (New England Biolabs)
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New England Biolabs nebnext rrna depletion 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 <t>sheep</t> <t>IgG-specific</t> 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.
Nebnext Rrna Depletion Kit, supplied by New England Biolabs, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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nebnext globin rrna depletion kit human mouse rat  (New England Biolabs)
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New England Biolabs nebnext globin rrna depletion kit human mouse rat
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 <t>sheep</t> <t>IgG-specific</t> 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.
Nebnext Globin Rrna Depletion Kit Human Mouse Rat, supplied by New England Biolabs, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


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: IgG levels in cell culture supernatants were detected by using a rat IgG ELISA kit (Aviva Systems Biology, San Diego, CA) according to the manufacturer’s instruction.

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