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rabbit anti cb  (Proteintech)


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    Structured Review

    Proteintech rabbit anti cb
    Rabbit Anti Cb, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 55 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+anti+cb/Calbindin-D28k+Antibody/pm41844620-394-35-39
    Average 94 stars, based on 55 article reviews
    rabbit anti cb - by Bioz Stars, 2026-09
    94/100 stars

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    Related Articles

    Immunohistochemistry:

    Article Title: Bidirectional regulation of social memory by two distinct types of GABAergic neurons in the lateral septum.
    Article Snippet: Brains were dissected and post-fixed in 4% PFA for 6 h at 4 °C, then immersed in 30% sucrose for 2 days before sectioning (30 μm) on a cryostat (Leica CM1050; Leica Biosystems, Germany). .. For IHC, slices were pre-incubated in blocking solution (10% normal goat serum with 0.3% Triton X-100 in PBS) for 1 h at room temperature (RT) and incubated overnight at 4 °C with primary antibodies, including rabbit anti-CB (1:500, #14479-1-AP; Proteintech, China), mouse anti-NeuN (1:1 000, #MAB377; Merck, Germany), guinea pig anti-c-fos (1:1 000, #226004; SYSY, Germany), rabbit anti-RGS14 (1:1 000, #16258-1-AP; Proteintech, China), rat antimCherry (1:1 000, #M11217; Thermo Fisher Scientific, USA), and rabbit anti-GFP (1:1 000, #A-11122; Thermo Fisher Scientific). .. The slices were washed in PBS (10 min, three times) and incubated with secondary antibodies (1:1 000, goat anti-rabbit Alexa Fluor 488, goat anti-rat Alexa Fluor 546, goat antiguinea pig Alexa Fluor 633, and goat anti-mouse Alexa Fluor 647; Invitrogen, USA) for 2 h at RT.

    Blocking Assay:

    Article Title: Bidirectional regulation of social memory by two distinct types of GABAergic neurons in the lateral septum.
    Article Snippet: Brains were dissected and post-fixed in 4% PFA for 6 h at 4 °C, then immersed in 30% sucrose for 2 days before sectioning (30 μm) on a cryostat (Leica CM1050; Leica Biosystems, Germany). .. For IHC, slices were pre-incubated in blocking solution (10% normal goat serum with 0.3% Triton X-100 in PBS) for 1 h at room temperature (RT) and incubated overnight at 4 °C with primary antibodies, including rabbit anti-CB (1:500, #14479-1-AP; Proteintech, China), mouse anti-NeuN (1:1 000, #MAB377; Merck, Germany), guinea pig anti-c-fos (1:1 000, #226004; SYSY, Germany), rabbit anti-RGS14 (1:1 000, #16258-1-AP; Proteintech, China), rat antimCherry (1:1 000, #M11217; Thermo Fisher Scientific, USA), and rabbit anti-GFP (1:1 000, #A-11122; Thermo Fisher Scientific). .. The slices were washed in PBS (10 min, three times) and incubated with secondary antibodies (1:1 000, goat anti-rabbit Alexa Fluor 488, goat anti-rat Alexa Fluor 546, goat antiguinea pig Alexa Fluor 633, and goat anti-mouse Alexa Fluor 647; Invitrogen, USA) for 2 h at RT.

    Incubation:

    Article Title: Bidirectional regulation of social memory by two distinct types of GABAergic neurons in the lateral septum.
    Article Snippet: Brains were dissected and post-fixed in 4% PFA for 6 h at 4 °C, then immersed in 30% sucrose for 2 days before sectioning (30 μm) on a cryostat (Leica CM1050; Leica Biosystems, Germany). .. For IHC, slices were pre-incubated in blocking solution (10% normal goat serum with 0.3% Triton X-100 in PBS) for 1 h at room temperature (RT) and incubated overnight at 4 °C with primary antibodies, including rabbit anti-CB (1:500, #14479-1-AP; Proteintech, China), mouse anti-NeuN (1:1 000, #MAB377; Merck, Germany), guinea pig anti-c-fos (1:1 000, #226004; SYSY, Germany), rabbit anti-RGS14 (1:1 000, #16258-1-AP; Proteintech, China), rat antimCherry (1:1 000, #M11217; Thermo Fisher Scientific, USA), and rabbit anti-GFP (1:1 000, #A-11122; Thermo Fisher Scientific). .. The slices were washed in PBS (10 min, three times) and incubated with secondary antibodies (1:1 000, goat anti-rabbit Alexa Fluor 488, goat anti-rat Alexa Fluor 546, goat antiguinea pig Alexa Fluor 633, and goat anti-mouse Alexa Fluor 647; Invitrogen, USA) for 2 h at RT.



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    ECS components are progressively dysregulated in human ADPKD kidney tissue. a Microarray analysis ( GSE7869 ) of human kidney tissue shows stepwise increases in CNR1 transcript from healthy cortex to minimally cystic (PKDm) and fully cystic (PKD) ADPKD tissue, with corresponding reductions in AEA-metabolizing enzymes NAPEPLD and FAAH . b Single-nucleus RNA-sequencing (snRNA-seq) analysis of human ADPKD kidneys ( n = 8) versus healthy controls ( n = 5) demonstrate consistent CNR1 upregulation and marked downregulation of NAPEPLD and FAAH , while 2-AG-metabolizing enzymes remain largely unchanged. c snRNA-seq analysis of diabetic kidney disease (DKD; n = 5 patients; controls n = 6) reveals minimal alterations in CNR1 and ECS-metabolizing enzymes. d Gene expression analysis by qPCR confirms CNR1 upregulation in human ADPKD kidney tissue ( n = 17) versus non-cystic nephrectomy controls ( n = 5), with concurrent changes in ECS enzyme transcription. e-i eCB quantification by liquid chromatography-tandem mass spectrometry (LC–MS/MS) reveals significant depletion of tissue anandamide (AEA); e , N -oleoylethanolamine (OEA); f , 2-arachidonoylglycerol (2-AG); h , and arachidonic acid (AA); i , while N -palmitoylethanolamine (PEA); g remains unchanged. j-l Western blot analysis shows substantial inter-individual variability in <t>CB</t> <t>1</t> <t>R</t> protein levels without significant difference between ADPKD ( n = 6) and control kidneys ( n = 4), but significant reductions in DAGLα/β, NAPEPLD, MGLL and FAAH protein. Western blots were normalized to total proteins. Data represent mean ± SEM. Statistics of control versus PKD represented by * and control versus PKDm by #. Statistical significance assessed by Mann–Whitney U test or unpaired t -test: * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
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    ECS components are progressively dysregulated in human ADPKD kidney tissue. a Microarray analysis ( GSE7869 ) of human kidney tissue shows stepwise increases in CNR1 transcript from healthy cortex to minimally cystic (PKDm) and fully cystic (PKD) ADPKD tissue, with corresponding reductions in AEA-metabolizing enzymes NAPEPLD and FAAH . b Single-nucleus RNA-sequencing (snRNA-seq) analysis of human ADPKD kidneys ( n = 8) versus healthy controls ( n = 5) demonstrate consistent CNR1 upregulation and marked downregulation of NAPEPLD and FAAH , while 2-AG-metabolizing enzymes remain largely unchanged. c snRNA-seq analysis of diabetic kidney disease (DKD; n = 5 patients; controls n = 6) reveals minimal alterations in CNR1 and ECS-metabolizing enzymes. d Gene expression analysis by qPCR confirms CNR1 upregulation in human ADPKD kidney tissue ( n = 17) versus non-cystic nephrectomy controls ( n = 5), with concurrent changes in ECS enzyme transcription. e-i eCB quantification by liquid chromatography-tandem mass spectrometry (LC–MS/MS) reveals significant depletion of tissue anandamide (AEA); e , N -oleoylethanolamine (OEA); f , 2-arachidonoylglycerol (2-AG); h , and arachidonic acid (AA); i , while N -palmitoylethanolamine (PEA); g remains unchanged. j-l Western blot analysis shows substantial inter-individual variability in <t>CB</t> <t>1</t> <t>R</t> protein levels without significant difference between ADPKD ( n = 6) and control kidneys ( n = 4), but significant reductions in DAGLα/β, NAPEPLD, MGLL and FAAH protein. Western blots were normalized to total proteins. Data represent mean ± SEM. Statistics of control versus PKD represented by * and control versus PKDm by #. Statistical significance assessed by Mann–Whitney U test or unpaired t -test: * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
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    ECS components are progressively dysregulated in human ADPKD kidney tissue. a Microarray analysis ( GSE7869 ) of human kidney tissue shows stepwise increases in CNR1 transcript from healthy cortex to minimally cystic (PKDm) and fully cystic (PKD) ADPKD tissue, with corresponding reductions in AEA-metabolizing enzymes NAPEPLD and FAAH . b Single-nucleus RNA-sequencing (snRNA-seq) analysis of human ADPKD kidneys ( n = 8) versus healthy controls ( n = 5) demonstrate consistent CNR1 upregulation and marked downregulation of NAPEPLD and FAAH , while 2-AG-metabolizing enzymes remain largely unchanged. c snRNA-seq analysis of diabetic kidney disease (DKD; n = 5 patients; controls n = 6) reveals minimal alterations in CNR1 and ECS-metabolizing enzymes. d Gene expression analysis by qPCR confirms CNR1 upregulation in human ADPKD kidney tissue ( n = 17) versus non-cystic nephrectomy controls ( n = 5), with concurrent changes in ECS enzyme transcription. e-i eCB quantification by liquid chromatography-tandem mass spectrometry (LC–MS/MS) reveals significant depletion of tissue anandamide (AEA); e , N -oleoylethanolamine (OEA); f , 2-arachidonoylglycerol (2-AG); h , and arachidonic acid (AA); i , while N -palmitoylethanolamine (PEA); g remains unchanged. j-l Western blot analysis shows substantial inter-individual variability in <t>CB</t> <t>1</t> <t>R</t> protein levels without significant difference between ADPKD ( n = 6) and control kidneys ( n = 4), but significant reductions in DAGLα/β, NAPEPLD, MGLL and FAAH protein. Western blots were normalized to total proteins. Data represent mean ± SEM. Statistics of control versus PKD represented by * and control versus PKDm by #. Statistical significance assessed by Mann–Whitney U test or unpaired t -test: * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
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    ECS components are progressively dysregulated in human ADPKD kidney tissue. a Microarray analysis ( GSE7869 ) of human kidney tissue shows stepwise increases in CNR1 transcript from healthy cortex to minimally cystic (PKDm) and fully cystic (PKD) ADPKD tissue, with corresponding reductions in AEA-metabolizing enzymes NAPEPLD and FAAH . b Single-nucleus RNA-sequencing (snRNA-seq) analysis of human ADPKD kidneys ( n = 8) versus healthy controls ( n = 5) demonstrate consistent CNR1 upregulation and marked downregulation of NAPEPLD and FAAH , while 2-AG-metabolizing enzymes remain largely unchanged. c snRNA-seq analysis of diabetic kidney disease (DKD; n = 5 patients; controls n = 6) reveals minimal alterations in CNR1 and ECS-metabolizing enzymes. d Gene expression analysis by qPCR confirms CNR1 upregulation in human ADPKD kidney tissue ( n = 17) versus non-cystic nephrectomy controls ( n = 5), with concurrent changes in ECS enzyme transcription. e-i eCB quantification by liquid chromatography-tandem mass spectrometry (LC–MS/MS) reveals significant depletion of tissue anandamide (AEA); e , N -oleoylethanolamine (OEA); f , 2-arachidonoylglycerol (2-AG); h , and arachidonic acid (AA); i , while N -palmitoylethanolamine (PEA); g remains unchanged. j-l Western blot analysis shows substantial inter-individual variability in <t>CB</t> <t>1</t> <t>R</t> protein levels without significant difference between ADPKD ( n = 6) and control kidneys ( n = 4), but significant reductions in DAGLα/β, NAPEPLD, MGLL and FAAH protein. Western blots were normalized to total proteins. Data represent mean ± SEM. Statistics of control versus PKD represented by * and control versus PKDm by #. Statistical significance assessed by Mann–Whitney U test or unpaired t -test: * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
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    ECS components are progressively dysregulated in human ADPKD kidney tissue. a Microarray analysis ( GSE7869 ) of human kidney tissue shows stepwise increases in CNR1 transcript from healthy cortex to minimally cystic (PKDm) and fully cystic (PKD) ADPKD tissue, with corresponding reductions in AEA-metabolizing enzymes NAPEPLD and FAAH . b Single-nucleus RNA-sequencing (snRNA-seq) analysis of human ADPKD kidneys ( n = 8) versus healthy controls ( n = 5) demonstrate consistent CNR1 upregulation and marked downregulation of NAPEPLD and FAAH , while 2-AG-metabolizing enzymes remain largely unchanged. c snRNA-seq analysis of diabetic kidney disease (DKD; n = 5 patients; controls n = 6) reveals minimal alterations in CNR1 and ECS-metabolizing enzymes. d Gene expression analysis by qPCR confirms CNR1 upregulation in human ADPKD kidney tissue ( n = 17) versus non-cystic nephrectomy controls ( n = 5), with concurrent changes in ECS enzyme transcription. e-i eCB quantification by liquid chromatography-tandem mass spectrometry (LC–MS/MS) reveals significant depletion of tissue anandamide (AEA); e , N -oleoylethanolamine (OEA); f , 2-arachidonoylglycerol (2-AG); h , and arachidonic acid (AA); i , while N -palmitoylethanolamine (PEA); g remains unchanged. j-l Western blot analysis shows substantial inter-individual variability in <t>CB</t> <t>1</t> <t>R</t> protein levels without significant difference between ADPKD ( n = 6) and control kidneys ( n = 4), but significant reductions in DAGLα/β, NAPEPLD, MGLL and FAAH protein. Western blots were normalized to total proteins. Data represent mean ± SEM. Statistics of control versus PKD represented by * and control versus PKDm by #. Statistical significance assessed by Mann–Whitney U test or unpaired t -test: * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
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    Cayman Chemical ab303556 rabbit anti cb 1 r cayman chemical
    ECS components are progressively dysregulated in human ADPKD kidney tissue. a Microarray analysis ( GSE7869 ) of human kidney tissue shows stepwise increases in CNR1 transcript from healthy cortex to minimally cystic (PKDm) and fully cystic (PKD) ADPKD tissue, with corresponding reductions in AEA-metabolizing enzymes NAPEPLD and FAAH . b Single-nucleus RNA-sequencing (snRNA-seq) analysis of human ADPKD kidneys ( n = 8) versus healthy controls ( n = 5) demonstrate consistent CNR1 upregulation and marked downregulation of NAPEPLD and FAAH , while 2-AG-metabolizing enzymes remain largely unchanged. c snRNA-seq analysis of diabetic kidney disease (DKD; n = 5 patients; controls n = 6) reveals minimal alterations in CNR1 and ECS-metabolizing enzymes. d Gene expression analysis by qPCR confirms CNR1 upregulation in human ADPKD kidney tissue ( n = 17) versus non-cystic nephrectomy controls ( n = 5), with concurrent changes in ECS enzyme transcription. e-i eCB quantification by liquid chromatography-tandem mass spectrometry (LC–MS/MS) reveals significant depletion of tissue anandamide (AEA); e , N -oleoylethanolamine (OEA); f , 2-arachidonoylglycerol (2-AG); h , and arachidonic acid (AA); i , while N -palmitoylethanolamine (PEA); g remains unchanged. j-l Western blot analysis shows substantial inter-individual variability in <t>CB</t> <t>1</t> <t>R</t> protein levels without significant difference between ADPKD ( n = 6) and control kidneys ( n = 4), but significant reductions in DAGLα/β, NAPEPLD, MGLL and FAAH protein. Western blots were normalized to total proteins. Data represent mean ± SEM. Statistics of control versus PKD represented by * and control versus PKDm by #. Statistical significance assessed by Mann–Whitney U test or unpaired t -test: * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
    Ab303556 Rabbit Anti Cb 1 R Cayman Chemical, supplied by Cayman Chemical, 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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    Image Search Results


    ECS components are progressively dysregulated in human ADPKD kidney tissue. a Microarray analysis ( GSE7869 ) of human kidney tissue shows stepwise increases in CNR1 transcript from healthy cortex to minimally cystic (PKDm) and fully cystic (PKD) ADPKD tissue, with corresponding reductions in AEA-metabolizing enzymes NAPEPLD and FAAH . b Single-nucleus RNA-sequencing (snRNA-seq) analysis of human ADPKD kidneys ( n = 8) versus healthy controls ( n = 5) demonstrate consistent CNR1 upregulation and marked downregulation of NAPEPLD and FAAH , while 2-AG-metabolizing enzymes remain largely unchanged. c snRNA-seq analysis of diabetic kidney disease (DKD; n = 5 patients; controls n = 6) reveals minimal alterations in CNR1 and ECS-metabolizing enzymes. d Gene expression analysis by qPCR confirms CNR1 upregulation in human ADPKD kidney tissue ( n = 17) versus non-cystic nephrectomy controls ( n = 5), with concurrent changes in ECS enzyme transcription. e-i eCB quantification by liquid chromatography-tandem mass spectrometry (LC–MS/MS) reveals significant depletion of tissue anandamide (AEA); e , N -oleoylethanolamine (OEA); f , 2-arachidonoylglycerol (2-AG); h , and arachidonic acid (AA); i , while N -palmitoylethanolamine (PEA); g remains unchanged. j-l Western blot analysis shows substantial inter-individual variability in CB 1 R protein levels without significant difference between ADPKD ( n = 6) and control kidneys ( n = 4), but significant reductions in DAGLα/β, NAPEPLD, MGLL and FAAH protein. Western blots were normalized to total proteins. Data represent mean ± SEM. Statistics of control versus PKD represented by * and control versus PKDm by #. Statistical significance assessed by Mann–Whitney U test or unpaired t -test: * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Journal: Molecular Medicine

    Article Title: Progressive endocannabinoid system dysregulation in autosomal dominant polycystic kidney disease

    doi: 10.1186/s10020-026-01457-w

    Figure Lengend Snippet: ECS components are progressively dysregulated in human ADPKD kidney tissue. a Microarray analysis ( GSE7869 ) of human kidney tissue shows stepwise increases in CNR1 transcript from healthy cortex to minimally cystic (PKDm) and fully cystic (PKD) ADPKD tissue, with corresponding reductions in AEA-metabolizing enzymes NAPEPLD and FAAH . b Single-nucleus RNA-sequencing (snRNA-seq) analysis of human ADPKD kidneys ( n = 8) versus healthy controls ( n = 5) demonstrate consistent CNR1 upregulation and marked downregulation of NAPEPLD and FAAH , while 2-AG-metabolizing enzymes remain largely unchanged. c snRNA-seq analysis of diabetic kidney disease (DKD; n = 5 patients; controls n = 6) reveals minimal alterations in CNR1 and ECS-metabolizing enzymes. d Gene expression analysis by qPCR confirms CNR1 upregulation in human ADPKD kidney tissue ( n = 17) versus non-cystic nephrectomy controls ( n = 5), with concurrent changes in ECS enzyme transcription. e-i eCB quantification by liquid chromatography-tandem mass spectrometry (LC–MS/MS) reveals significant depletion of tissue anandamide (AEA); e , N -oleoylethanolamine (OEA); f , 2-arachidonoylglycerol (2-AG); h , and arachidonic acid (AA); i , while N -palmitoylethanolamine (PEA); g remains unchanged. j-l Western blot analysis shows substantial inter-individual variability in CB 1 R protein levels without significant difference between ADPKD ( n = 6) and control kidneys ( n = 4), but significant reductions in DAGLα/β, NAPEPLD, MGLL and FAAH protein. Western blots were normalized to total proteins. Data represent mean ± SEM. Statistics of control versus PKD represented by * and control versus PKDm by #. Statistical significance assessed by Mann–Whitney U test or unpaired t -test: * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Article Snippet: Sections were stained with rabbit anti-CB 1 R antibody (1:200, 10006590, Cayman) followed by a goat anti-rabbit HRP conjugate (ImmPRESSTM, Vector laboratories).

    Techniques: Microarray, RNA Sequencing, Gene Expression, Liquid Chromatography, Mass Spectrometry, Liquid Chromatography with Mass Spectroscopy, Western Blot, Control, MANN-WHITNEY

    Temporal endocannabinoid system dysregulation during Pkd1 RC/RC disease progression. a-g Quantitative PCR analysis of ECS-related genes across disease stages (9 and 12 months) showing progressive upregulation of Cnr1 a and Cnr2 b transcripts, with corresponding changes in ECS metabolic enzymes: Dagla c , Daglb d , Napepld e , Mgll f , and Faah g . h-n Western blot analysis and quantification of ECS proteins across disease stages, demonstrating sustained CB 1 R protein elevation at 9 and 12 months h, i , stable 2-AG-related enzyme proteins (DAGLα, DAGLβ, MGLL; h, j, k, m ), and stage-specific changes in AEA-related enzymes including elevated NAPEPLD at 12 months ( h, l ) and reduced FAAH at 9 months ( h, n ). Data represent mean ± SEM from WT ( n = 5) and Pkd1 RC/RC ( n = 6–7) per group per timepoint. Statistical analysis: unpaired t -test comparing Pkd1 RC/RC to age-matched WT. Statistical significance: * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 versus WT

    Journal: Molecular Medicine

    Article Title: Progressive endocannabinoid system dysregulation in autosomal dominant polycystic kidney disease

    doi: 10.1186/s10020-026-01457-w

    Figure Lengend Snippet: Temporal endocannabinoid system dysregulation during Pkd1 RC/RC disease progression. a-g Quantitative PCR analysis of ECS-related genes across disease stages (9 and 12 months) showing progressive upregulation of Cnr1 a and Cnr2 b transcripts, with corresponding changes in ECS metabolic enzymes: Dagla c , Daglb d , Napepld e , Mgll f , and Faah g . h-n Western blot analysis and quantification of ECS proteins across disease stages, demonstrating sustained CB 1 R protein elevation at 9 and 12 months h, i , stable 2-AG-related enzyme proteins (DAGLα, DAGLβ, MGLL; h, j, k, m ), and stage-specific changes in AEA-related enzymes including elevated NAPEPLD at 12 months ( h, l ) and reduced FAAH at 9 months ( h, n ). Data represent mean ± SEM from WT ( n = 5) and Pkd1 RC/RC ( n = 6–7) per group per timepoint. Statistical analysis: unpaired t -test comparing Pkd1 RC/RC to age-matched WT. Statistical significance: * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 versus WT

    Article Snippet: Sections were stained with rabbit anti-CB 1 R antibody (1:200, 10006590, Cayman) followed by a goat anti-rabbit HRP conjugate (ImmPRESSTM, Vector laboratories).

    Techniques: Biomarker Discovery, Real-time Polymerase Chain Reaction, Western Blot