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rabbit anti calbindin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti calbindin
    Rabbit Anti Calbindin, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+anti+calbindin/pmc13000480-346-49-53
    Average 86 stars, based on 1 article reviews
    rabbit anti calbindin - by Bioz Stars, 2026-09
    86/100 stars

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    Related Articles

    Blocking Assay:

    Article Title: Antibody-assisted selective isolation of Purkinje cell nuclei from mouse cerebellar tissue.
    Article Snippet: .. Blocking was performed with 5%BSA in PBS at room temperature for 1 h. Next, the slices were stained overnight at 4 Cwith primary antibodies: rabbit anti-calbindin (1:400, Cat. No. 13176, Cell Signaling) and mouse anti-Myc-Tag (1:200 Cat. No. 2276, Cell Signaling). .. After another round of washing (three times in PBS for 10 min each), the slices were stained with secondary fluorescent goat anti-mouse and rabbit antibodies (1:400 each, Cat No. A28175 and A11012, Thermo Fisher Scientific).

    Article Title: Antibody-assisted selective isolation of Purkinje cell nuclei from mouse cerebellar tissue
    Article Snippet: .. Blocking was performed with 5% BSA in PBS at room temperature for 1 h. Next, the slices were stained overnight at 4°C with primary antibodies: rabbit anti-calbindin (1:400, Cat. No. 13176, Cell Signaling) and mouse anti-Myc-Tag (1:200 Cat. No. 2276, Cell Signaling). .. After another round of washing (three times in PBS for 10 min each), the slices were stained with secondary fluorescent goat anti-mouse and rabbit antibodies (1:400 each, Cat No. A28175 and A11012, Thermo Fisher Scientific).

    Article Title: Defective Astrocyte Maturation Drives Cerebellar Neuroinflammation and Degeneration
    Article Snippet: Subsequently, brains were embedded in optimal cutting medium (Tissue- Tek, VWR), and 50 μm frozen sections were prepared on probe plus microscopy slides (Fisher Sci). .. For permeabilization, a solution of 1% Triton X- 100in PBS was applied for 1 h, followed by blocking in PBS containing 0.5% Triton X- 100 and fish skin gelatin (Electron Microscopy) for 1 h. Primary antibodies Chicken Anti- GFAP (Aves Lab., GFAP, 1:500), Rabbit Anti- IBA1 (FUJIFILM, 016- 20001, 1:200), Rabbit Anti- β- Catenin (Millipore, ABE208, 1:200), Rabbit Anti- NeuN (Cell Signaling Tech., D4G40, 1:200), Rabbit Anti- Calbindin (Cell Signaling Tech., D1I4Q, 1:200), Mouse Anti- APC (CC1) (Millipore, OP80, 1:200), Rabbit Anti- GLAST (Cell Signaling Tech., D44E2, 1:200), Guinea Pig Anti- GLT1 (Millipore, AB1783, 1:200), Rabbit Anti- Aquaporin (CiteAB, AQP- 004, 1:200), Rabbit Anti- S100β (Cell Signaling Tech., E7C3A, 1:200), Guinea Pig Anti- VGLUT1 (Millipore, AB5605, 1:100), Guinea Pig AntiVGLUT2 (Millipore, AB2251- 1, 1:100) and Rabbit Anti- BLBP (Abcam, ab32423, 1:200) were diluted in the blocking buffer, applied onto slides, and incubated overnight at 4°C. .. Subsequently, sections underwent three washes before being exposed to the Alexa Fluor- 488, −594, or −633 labeled secondary antibodies (diluted at 1:1000, Invitrogen) for 45 min at 37°C.

    Staining:

    Article Title: Antibody-assisted selective isolation of Purkinje cell nuclei from mouse cerebellar tissue.
    Article Snippet: .. Blocking was performed with 5%BSA in PBS at room temperature for 1 h. Next, the slices were stained overnight at 4 Cwith primary antibodies: rabbit anti-calbindin (1:400, Cat. No. 13176, Cell Signaling) and mouse anti-Myc-Tag (1:200 Cat. No. 2276, Cell Signaling). .. After another round of washing (three times in PBS for 10 min each), the slices were stained with secondary fluorescent goat anti-mouse and rabbit antibodies (1:400 each, Cat No. A28175 and A11012, Thermo Fisher Scientific).

    Article Title: Antibody-assisted selective isolation of Purkinje cell nuclei from mouse cerebellar tissue
    Article Snippet: .. Blocking was performed with 5% BSA in PBS at room temperature for 1 h. Next, the slices were stained overnight at 4°C with primary antibodies: rabbit anti-calbindin (1:400, Cat. No. 13176, Cell Signaling) and mouse anti-Myc-Tag (1:200 Cat. No. 2276, Cell Signaling). .. After another round of washing (three times in PBS for 10 min each), the slices were stained with secondary fluorescent goat anti-mouse and rabbit antibodies (1:400 each, Cat No. A28175 and A11012, Thermo Fisher Scientific).

    Article Title: Cerebellar microglia-derived IL-17A mitigates autism-related behavioral and synaptic deficits.
    Article Snippet: .. The slices were stained overnight at 4 °C with primary antibodies, including rabbit anti-Iba1 (1:500, Wako, Cat# 016-20001), mouse anti-IL17A (1:100, eBioscience, Cat# 14-7179-82), goat anti-IL17RA (1:200, R&D, Cat# AF448), rabbit anti-Calbindin (1:500, Cell Signaling Technology, Cat# 13176), mouse anti-Calbindin (1:200, Proteintech, Cat# 66394-1-Ig), rabbit anti-S100β (1:200, Abcam, Cat# ab52642), anti-mouseCD3-AP3 (1:100, BioLegand, Cat# 100311), and rabbit anti-arc (1:500, Proteintech, Cat# 16290-1-AP), rabbit anti-phospho-NF-κB p65 (Ser536) (1:200, Cell Signaling Technology, Cat# 3033), mouse anti-Gephyrin (1:500, Synaptic Systems, Cat# 147008), and rabbit anti-GABAAR α1 (1:200, Synaptic Systems, Cat# 2224203). ..

    Incubation:

    Article Title: Neonatal hyperoxia exposure causes cerebellar lesions and behavioral abnormalities in rats.
    Article Snippet: .. Subsequently, the 528 sections were incubated overnight at 4°C with monoclonal rat anti-BrdU 529 (1:1,000 in PBS, Bio-Rad Laboratories, Hercules, CA), rat anti-MBP (1:200 in 530 PBS, Merck Millipore, Burlington, MA), or rabbit anti-Calbindin (1:400 in PBS, 531 Cell Signaling Technology, Danvers, MA) antibodies. .. The sections were 532 subsequently incubated with appropriate biotinylated secondary antibodies 533 (Vector Laboratories, Newark, CA) for 60 min at room temperature.

    Article Title: Defective Astrocyte Maturation Drives Cerebellar Neuroinflammation and Degeneration
    Article Snippet: Subsequently, brains were embedded in optimal cutting medium (Tissue- Tek, VWR), and 50 μm frozen sections were prepared on probe plus microscopy slides (Fisher Sci). .. For permeabilization, a solution of 1% Triton X- 100in PBS was applied for 1 h, followed by blocking in PBS containing 0.5% Triton X- 100 and fish skin gelatin (Electron Microscopy) for 1 h. Primary antibodies Chicken Anti- GFAP (Aves Lab., GFAP, 1:500), Rabbit Anti- IBA1 (FUJIFILM, 016- 20001, 1:200), Rabbit Anti- β- Catenin (Millipore, ABE208, 1:200), Rabbit Anti- NeuN (Cell Signaling Tech., D4G40, 1:200), Rabbit Anti- Calbindin (Cell Signaling Tech., D1I4Q, 1:200), Mouse Anti- APC (CC1) (Millipore, OP80, 1:200), Rabbit Anti- GLAST (Cell Signaling Tech., D44E2, 1:200), Guinea Pig Anti- GLT1 (Millipore, AB1783, 1:200), Rabbit Anti- Aquaporin (CiteAB, AQP- 004, 1:200), Rabbit Anti- S100β (Cell Signaling Tech., E7C3A, 1:200), Guinea Pig Anti- VGLUT1 (Millipore, AB5605, 1:100), Guinea Pig AntiVGLUT2 (Millipore, AB2251- 1, 1:100) and Rabbit Anti- BLBP (Abcam, ab32423, 1:200) were diluted in the blocking buffer, applied onto slides, and incubated overnight at 4°C. .. Subsequently, sections underwent three washes before being exposed to the Alexa Fluor- 488, −594, or −633 labeled secondary antibodies (diluted at 1:1000, Invitrogen) for 45 min at 37°C.

    Article Title: Reduced SK channel control of mesolimbic dopamine neuron firing drives reward seeking adaptations in chronic pain
    Article Snippet: .. Slices were then incubated with rabbit anti-calbindin (1:200, Cell Signaling Technology, 13176) and mouse anti-TH (1:500, Sigma-Aldrich, T2928) with 3% normal donkey serum and 0.3% Triton-X-100 for 48 h at 4°C. .. Slices had 3 washes in PBS for 15 min and were then incubated in goat anti-mouse AlexaFluor 555 (1:1000, Thermo Fisher) and goat anti-rabbit AlexaFluor 488 (1:1000, Thermo Fisher) overnight at 4°C.

    Article Title: Neonatal hyperoxia exposure causes cerebellar lesions and behavioral abnormalities in rats
    Article Snippet: .. Subsequently, the sections were incubated overnight at 4 °C with monoclonal rat anti-BrdU (1:1,000 in PBS, Bio-Rad Laboratories, Hercules, CA), rat anti-MBP (1:200 in PBS, Merck Millipore, Burlington, MA), or rabbit anti-Calbindin (1:400 in PBS, Cell Signaling Technology, Danvers, MA) antibodies. .. The sections were subsequently incubated with appropriate biotinylated secondary antibodies (Vector Laboratories, Newark, CA) for 60 min at room temperature.

    Binding Assay:

    Article Title: Dual mechanisms of supporting cell regeneration in the neonatal mouse cochlea
    Article Snippet: Tissues were washed another three times with PBS at 10-minute intervals and mounted with ProLong Gold Antifade Mountant (Invitrogen) then coverslipped. .. The following primary antibodies were used: goat anti-Sox2 (1:200; R&D Systems), rabbit anti-fatty acid binding protein 7 (FABP7, 1:200, Abcam), mouse anti-Connexin 26 (1:400; Thermo Fisher), rabbit anti-EAAT1/GLAST (1:500; Abcam), rat anti-ki67 (1:100; Thermo Fisher), rabbit anti-cellular retinoic acid binding protein 1 (CRABP1, 1:200, VWR-Proteintech), goat anti-Galectin-1 (1:50, R&D), rabbit anti-calbindin (Calb1, 1:200, Cell Signaling Technologies), goat anti-Jagged1 (1:100, Santa Cruz). .. Alexa Fluor secondary antibodies (488, 546, 1:500, Invitrogen) were used.

    Electron Microscopy:

    Article Title: Defective Astrocyte Maturation Drives Cerebellar Neuroinflammation and Degeneration
    Article Snippet: Subsequently, brains were embedded in optimal cutting medium (Tissue- Tek, VWR), and 50 μm frozen sections were prepared on probe plus microscopy slides (Fisher Sci). .. For permeabilization, a solution of 1% Triton X- 100in PBS was applied for 1 h, followed by blocking in PBS containing 0.5% Triton X- 100 and fish skin gelatin (Electron Microscopy) for 1 h. Primary antibodies Chicken Anti- GFAP (Aves Lab., GFAP, 1:500), Rabbit Anti- IBA1 (FUJIFILM, 016- 20001, 1:200), Rabbit Anti- β- Catenin (Millipore, ABE208, 1:200), Rabbit Anti- NeuN (Cell Signaling Tech., D4G40, 1:200), Rabbit Anti- Calbindin (Cell Signaling Tech., D1I4Q, 1:200), Mouse Anti- APC (CC1) (Millipore, OP80, 1:200), Rabbit Anti- GLAST (Cell Signaling Tech., D44E2, 1:200), Guinea Pig Anti- GLT1 (Millipore, AB1783, 1:200), Rabbit Anti- Aquaporin (CiteAB, AQP- 004, 1:200), Rabbit Anti- S100β (Cell Signaling Tech., E7C3A, 1:200), Guinea Pig Anti- VGLUT1 (Millipore, AB5605, 1:100), Guinea Pig AntiVGLUT2 (Millipore, AB2251- 1, 1:100) and Rabbit Anti- BLBP (Abcam, ab32423, 1:200) were diluted in the blocking buffer, applied onto slides, and incubated overnight at 4°C. .. Subsequently, sections underwent three washes before being exposed to the Alexa Fluor- 488, −594, or −633 labeled secondary antibodies (diluted at 1:1000, Invitrogen) for 45 min at 37°C.



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    ScRNA-seq reveals damage-induced transcriptomes of the greater epithelial ridge and inner phalangeal cells (A) UMAP showing integration of Epcam + cochlear epithelial cells from P4-P7 control ( Ki67 CreERT2/+ ; R26R tdTomato/+ ) and damage ( Ki67 CreERT2/+ ; Lgr5 DTR/+ ; R26R tdTomato/+ ) cochlea, resulting in 18 individual clusters. (B) UMAPs showing gene expression profiles of medial and lateral GER markers. (C) UMAPs showing cell clusters integrated from control and damage cochlea at individual time points. Arrows indicate cell clusters predominantly or exclusively found in the damaged cochlea. (D) Percent distribution of cells from each time point and condition by cluster. To account for differences in the number of profiled cells in each dataset, percent contribution to each cluster was normalized to the dataset size. Blue asterisk denotes proliferating GER cells, red asterisks denote native and responding DC/IPC populations. Note that cluster 10 (native DC/IPCs) are mainly composed of cells from control cochlea, whereas cluster 8 (responding DC/IPC) is entirely composed of cells from damaged cochlea. (E) UMAPs showing a reduction of Lgr5 + cells in the damaged cochlea, as well as an increase in Ki67-tdTomato + cells in the damaged lateral GER and Fabp3 + responding DC/IPCs. Cluster 17 (proliferating cells) express Mki67 . (F) Overlaid expression of “cell cycle” and “pathways of neurodegeneration—multiple diseases” gene signatures, extracted from KEGG Pathways mmu04110 and mmu05022 using clusterProfiler. Cell cycle gene signature is highly enriched in cluster 17 and moderately enriched in cluster 8. See also . (G) Volcano plots showing differentially expressed genes between damage and control GER and IPhC clusters at all four time points (excluding proliferating cell cluster). (H) Immunostaining showing that Galectin1 and <t>Calb1</t> mark medial GER (white brackets) in all three turns of the control cochlea (P6-7). After damage, domains expressing Galectin1 and Calb1 expand laterally into the central GER. Note that Calb1 also labels hair cells. (I) Crabp1 is expressed in medial GER in all three turns of P4 and P7 control cochlea. At P4 after damage, its expression robustly increased and expanded to the central and lateral GER, before returning to similar levels and spatial pattern as controls at P7. (J) Immunostaining shows that Jag1 expression initially decreases in the lateral GER relative to controls at P4, before upregulation at P7 to more intense levels than controls. (K) Quantification of Crabp1-expressing regions shows a significant increase after damage relative to controls at P7 ( n = 3). Unpaired t tests were used for (K). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Brackets represent GER. IHC = inner hair cell (arrows), OHC = outer hair cell, GER = greater epithelial ridge. Scale bars represent 50 μm.
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    Image Search Results


    ScRNA-seq reveals damage-induced transcriptomes of the greater epithelial ridge and inner phalangeal cells (A) UMAP showing integration of Epcam + cochlear epithelial cells from P4-P7 control ( Ki67 CreERT2/+ ; R26R tdTomato/+ ) and damage ( Ki67 CreERT2/+ ; Lgr5 DTR/+ ; R26R tdTomato/+ ) cochlea, resulting in 18 individual clusters. (B) UMAPs showing gene expression profiles of medial and lateral GER markers. (C) UMAPs showing cell clusters integrated from control and damage cochlea at individual time points. Arrows indicate cell clusters predominantly or exclusively found in the damaged cochlea. (D) Percent distribution of cells from each time point and condition by cluster. To account for differences in the number of profiled cells in each dataset, percent contribution to each cluster was normalized to the dataset size. Blue asterisk denotes proliferating GER cells, red asterisks denote native and responding DC/IPC populations. Note that cluster 10 (native DC/IPCs) are mainly composed of cells from control cochlea, whereas cluster 8 (responding DC/IPC) is entirely composed of cells from damaged cochlea. (E) UMAPs showing a reduction of Lgr5 + cells in the damaged cochlea, as well as an increase in Ki67-tdTomato + cells in the damaged lateral GER and Fabp3 + responding DC/IPCs. Cluster 17 (proliferating cells) express Mki67 . (F) Overlaid expression of “cell cycle” and “pathways of neurodegeneration—multiple diseases” gene signatures, extracted from KEGG Pathways mmu04110 and mmu05022 using clusterProfiler. Cell cycle gene signature is highly enriched in cluster 17 and moderately enriched in cluster 8. See also . (G) Volcano plots showing differentially expressed genes between damage and control GER and IPhC clusters at all four time points (excluding proliferating cell cluster). (H) Immunostaining showing that Galectin1 and Calb1 mark medial GER (white brackets) in all three turns of the control cochlea (P6-7). After damage, domains expressing Galectin1 and Calb1 expand laterally into the central GER. Note that Calb1 also labels hair cells. (I) Crabp1 is expressed in medial GER in all three turns of P4 and P7 control cochlea. At P4 after damage, its expression robustly increased and expanded to the central and lateral GER, before returning to similar levels and spatial pattern as controls at P7. (J) Immunostaining shows that Jag1 expression initially decreases in the lateral GER relative to controls at P4, before upregulation at P7 to more intense levels than controls. (K) Quantification of Crabp1-expressing regions shows a significant increase after damage relative to controls at P7 ( n = 3). Unpaired t tests were used for (K). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Brackets represent GER. IHC = inner hair cell (arrows), OHC = outer hair cell, GER = greater epithelial ridge. Scale bars represent 50 μm.

    Journal: iScience

    Article Title: Dual mechanisms of supporting cell regeneration in the neonatal mouse cochlea

    doi: 10.1016/j.isci.2026.115113

    Figure Lengend Snippet: ScRNA-seq reveals damage-induced transcriptomes of the greater epithelial ridge and inner phalangeal cells (A) UMAP showing integration of Epcam + cochlear epithelial cells from P4-P7 control ( Ki67 CreERT2/+ ; R26R tdTomato/+ ) and damage ( Ki67 CreERT2/+ ; Lgr5 DTR/+ ; R26R tdTomato/+ ) cochlea, resulting in 18 individual clusters. (B) UMAPs showing gene expression profiles of medial and lateral GER markers. (C) UMAPs showing cell clusters integrated from control and damage cochlea at individual time points. Arrows indicate cell clusters predominantly or exclusively found in the damaged cochlea. (D) Percent distribution of cells from each time point and condition by cluster. To account for differences in the number of profiled cells in each dataset, percent contribution to each cluster was normalized to the dataset size. Blue asterisk denotes proliferating GER cells, red asterisks denote native and responding DC/IPC populations. Note that cluster 10 (native DC/IPCs) are mainly composed of cells from control cochlea, whereas cluster 8 (responding DC/IPC) is entirely composed of cells from damaged cochlea. (E) UMAPs showing a reduction of Lgr5 + cells in the damaged cochlea, as well as an increase in Ki67-tdTomato + cells in the damaged lateral GER and Fabp3 + responding DC/IPCs. Cluster 17 (proliferating cells) express Mki67 . (F) Overlaid expression of “cell cycle” and “pathways of neurodegeneration—multiple diseases” gene signatures, extracted from KEGG Pathways mmu04110 and mmu05022 using clusterProfiler. Cell cycle gene signature is highly enriched in cluster 17 and moderately enriched in cluster 8. See also . (G) Volcano plots showing differentially expressed genes between damage and control GER and IPhC clusters at all four time points (excluding proliferating cell cluster). (H) Immunostaining showing that Galectin1 and Calb1 mark medial GER (white brackets) in all three turns of the control cochlea (P6-7). After damage, domains expressing Galectin1 and Calb1 expand laterally into the central GER. Note that Calb1 also labels hair cells. (I) Crabp1 is expressed in medial GER in all three turns of P4 and P7 control cochlea. At P4 after damage, its expression robustly increased and expanded to the central and lateral GER, before returning to similar levels and spatial pattern as controls at P7. (J) Immunostaining shows that Jag1 expression initially decreases in the lateral GER relative to controls at P4, before upregulation at P7 to more intense levels than controls. (K) Quantification of Crabp1-expressing regions shows a significant increase after damage relative to controls at P7 ( n = 3). Unpaired t tests were used for (K). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Brackets represent GER. IHC = inner hair cell (arrows), OHC = outer hair cell, GER = greater epithelial ridge. Scale bars represent 50 μm.

    Article Snippet: Rabbit anti-calbindin (Calb1) , Cell Signaling Technologies , Cat#13176: RRID: AB_2687400.

    Techniques: Control, Gene Expression, Expressing, Immunostaining