- MA1-06305 - Invitrogen Antibodies CDH6 antibody

Submitted references Angiotensin II induces coordinated calcium bursts in aldosterone-producing adrenal rosettes.

Guagliardo NA, Klein PM, Gancayco CA, Lu A, Leng S, Makarem RR, Cho C, Rusin CG, Breault DT, Barrett PQ, Beenhakker MP
Nature communications 2020 Apr 3;11(1):1679

In situ molecular characterization of endoneurial microvessels that form the blood-nerve barrier in normal human adult peripheral nerves.

Ouyang X, Dong C, Ubogu EE
Journal of the peripheral nervous system : JPNS 2019 Jun;24(2):195-206

miR-223-3p Inhibits Human Osteosarcoma Metastasis and Progression by Directly Targeting CDH6.

Ji Q, Xu X, Song Q, Xu Y, Tai Y, Goodman SB, Bi W, Xu M, Jiao S, Maloney WJ, Wang Y
Molecular therapy : the journal of the American Society of Gene Therapy 2018 May 2;26(5):1299-1312

Cadherin-6 is a putative tumor suppressor and target of epigenetically dysregulated miR-429 in cholangiocarcinoma.

Goeppert B, Ernst C, Baer C, Roessler S, Renner M, Mehrabi A, Hafezi M, Pathil A, Warth A, Stenzinger A, Weichert W, Bähr M, Will R, Schirmacher P, Plass C, Weichenhan D
Epigenetics 2016 Nov;11(11):780-790

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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Immunostaining of K-cadherin from human skin using Product # MA1-06305.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Immunohistochemistry on frozen section of human kidney: positive reactivity in renal tubules (epithelium) stained with Cadherin K monoclonal antibody (Product # MA1-06305).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Immunohistochemistry on paraffin section of human kidney stained with Cadherin K monoclonal antibody (Product # MA1-06305).

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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Endothelial cell-specific proteins. Representative indirect fluorescent digital photomicrographs of cryostat axial sections of normal adult sural nerves show UEA-1-positive endothelial cells (green; A, E, I, M) with expression of CLDN5, ESAM, MPDZ, and CDH6 (red; B, F, J, N, respectively) restricted to endoneurial microvessels and fenestrated epineurial macrovessels shown in the merged images at lower and higher magnifications (yellow/ orange). CDH6 is also expressed by large diameter axons (M-P). Expression of these proteins by both endoneurial microvascular and epineurial macrovascular endothelium suggests endothelial-specific, non-restrictive barrier functions at the normal adult human blood-nerve barrier. White arrows demonstrate positively staining endoneurial microvessels. Blue (4, 6-diamidino-2-phenylindole) staining indicates nuclei. Scale bar 500 mum for A-C, E-G, I-K, M-O, and 125 mum for D, H, L and P

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Experimental details: Fig. 7 Disruption of N-cadherin shortens burst duration without affecting other calcium spike parameters. a Immunohistochemistry showing N-cadherin (red, upper left), K-cadherin (red, lower left) and F-actin (green, middle) are abundant in the zG layer (right, merged images). Scale bar: 20 um. b Model of calcium switch assay: Disrupting adherins junctional complex by reducing extracellular calcium with EDTA. Anti-N/K-cadherin antibodies (EC-Abs) binds to the now exposed extracellular N- and K-cadherin binding sites, inhibiting reformation of strong cell-cell adhesion after calcium is restored. For controls, we substituted an antibody directed to the conserved intracellular domain (IC-Ab) of cadherins. c - f Adrenal slices were stimulated with 300 pM ( c , e ) or 3 nM ( d , f ) Ang II after 1.5 min of baseline recording. EC-Abs: n = 6; IC-Ab: n = 6. c , d Mean spikes per 1 min bin over a 10 min period; EC-Abs treated slices had fewer spikes over time for both 300 pM and 3 nM Ang II (2-way ANOVA, effect of antibody: P = 0.011 and 0.018, respectively) as well as mean fractional active time ( c , d insets, mean +- SEM: 300 pM: IC-Ab 0.40 +- 0.04, EC-Abs 0.22 +- 0.03; 3 nM: IC-Ab 0.48 +- 0.05, EC-Abs 0.26 +- 0.06; Wilcoxon rank test, * P = 0.016 and 0.016, respectively). e , f Reduced activity was due to a decrease in the number of bursts per cell ( e , f left panels; mean +- SEM: 300 pM: IC-Ab 5.43 +- 0.39, EC-Abs 4.35 +- 0.44; 3 nM: IC-Ab 6.94 +- 0.67, EC-Abs 4.8 +- 0.66; Wicoxo

Supportive validation

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Experimental details: Fig. 8 Cadherin disruption reduces both the number of clustered cells and the production of aldosterone. a Significantly fewer cells clustered after N/K EC-Abs treatment when stimulated with 300 pM or 3 nM Ang II (means +- SEM: 300 pM Ang II: IC-Ab 0.45 +- 0.19, EC-Abs 0.09 +- 0.06; 3 nM Ang II: IC-Ab 0.71 +- 0.20, EC-Abs 0.07 +- 0.04; 1-way ANOVA, 300 pM Ang II: * P = 0.026; 3 nM Ang II: *** P < 0.0001). b However, cells that remained in functional clusters were proximate (C: clustered; N-C: non-clustered; means +- SEM: 300 pM Ang II: IC-Ab-C 7.77 +- 0.50, IC-Ab-N-C 49.60 +- 4.89, EC-Abs-C 5.55 +- 1.85, EC-Abs-N-C 35.44 +- 3.78; 3 nM Ang II: IC-Ab-C 11.20 +- 1.02, IC-Ab-N-C 35.96 +- 4.13, EC-Abs-C 7.95 +- 0.58, EC-Abs-N-C 47.65 +- 6.30; 1-way ANOVA, 300pM Ang II: IC-Ab C vs C-N *** P < 0.0001, EC-Abs C vs C-N *** P < 0.0001; 3 nM Ang II: IC-Ab C vs C-N *** P = 0.0005, EC-Abs C vs C-N *** P < 0.0001) and c produced phase-locked calcium oscillations (smaller PD-STDEV). d PD-STDEV Notably, aldosterone production was reduced after N-/K-cadherin disruption, both at baseline and following 3 nM Ang II stimulation (means +- SEM: baseline: IC-Ab 1.00 +- 0.05 [ n = 23], EC-Abs 0.60 +- 0.04 [ n = 20]; 3 nM Ang II: IC-Ab 1.00 +- 0.04 [ n = 23], EC-Abs 0.70 +- 0.03 [ n = 20]; 1-way ANOVA, baseline: *** P < 0.0001; 3 nM Ang II: *** P < 0.0001). Each data point represents aldosterone secreted from slices within a well standardized to the mean production in control (IC-Ab) wells. Lines and

MA1-06305

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