36-4500

antibody from Invitrogen Antibodies

Targeting: CLDN11 OSP, OTM

Provider product page for 36-4500

Western blot

ELISA

Immunoprecipitation

Immunohistochemistry

Other assay

Antibody data

Antibody Data
Antigen structure
References [58]
Comments [0]
Validations
Immunohistochemistry [2]
Other assay [28]

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Product number: 36-4500 - Provider product page
Provider: Invitrogen Antibodies
Product name: Claudin 11 Polyclonal Antibody
Antibody type: Polyclonal
Antigen: Synthetic peptide
Reactivity: Human, Mouse
Host: Rabbit
Isotype: IgG
Vial size: 100 µg
Concentration: 0.25 mg/mL
Storage: -20°C

CLDN11 protein structure - 36-4500 shown in red.

Supportive validation

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Supportive validation

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Supportive validation

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Supportive validation

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Supportive validation

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Supportive validation

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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

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Experimental details: NULL

Supportive validation

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Experimental details: NULL

Supportive validation

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Experimental details: NULL

Supportive validation

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Experimental details: NULL

Supportive validation

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Experimental details: NULL

Supportive validation

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Experimental details: NULL

Supportive validation

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Supportive validation

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Experimental details: Figure 1 Nf1 Loss or HRas Activation in Oligodendrocytes Causes Optic-Nerve Enlargement, Myelin Decompaction, Loss of Claudin-11, and Altered Cx32 Localization (A) Gross micrographs of optic nerves at the level of the chiasm in 12-month-old animals. Ruler shows 1 mm markings. (B) Toluidine-blue-stained semithin optic-nerve cross-sections, 1 mm rostral to the chiasm. (C) Optic-nerve g-ratio scatterplots (~5,000 axons/graph; measurements 1 mm rostral to the chiasm in three to five electron micrographs at 10,000x). Red box: 99% of WT g-ratios superimposed upon graphs of other genotypes. ANOVA, Tukey post hoc, p = 2.2 x 10 -16 . (D) Diagram of myelin compaction. Brown circle: axon cross-section; gray: major dense lines (MDLs); orange: Cx32 GJs between compact myelin layers; blue lines: claudin-11+ TJs in compact myelin. (E) Electron micrographs (scale bar, 10 nm) of WT, PLPCre;Nf1 fl / fl , and CNP-HRas optic-nerve myelin. White arrows: intraperiod lines (ILs); black arrows: MDLs. (F-I) Western blots of total optic-nerve lysate or whole-brain cytosolic, endosomal, or myelin fractions showing myelin proteins (F), claudin-11 (G), or Cx32 cellular localization (H and I). n = 3-5 animals/genotype/experiment. See also Figures S1, S2, S3, and S4 .

Supportive validation

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Experimental details: FIGURE 2: Msi-1 knockdown by RNAi in Sertoli cells perturbs Sertoli cell-cell junctions via changes in BTB-associated proteins. (A) On day 3, Sertoli cells were transfected with Msi-1-specific siRNA duplexes and nontargeting control siRNA duplexes. The TER was detected until day 7, and each data point is the mean +- SD of n = 5 replicates from a representative experiment. *, p < 0.05. (B) Immunoblot showing the steady-state levels of Msi-1, basal ectoplasmic specialization (ES) proteins, and TJ proteins in lysates of Sertoli cells lysed 48 h after transfection; beta-tubulin served as a loading control. (C) Histogram summarizing selected immunoblotting results in B and normalized against beta-tubulin. Each bar represents the mean +- SD of n = 3 experiments. *, p < 0.05. (D-F) Changes in the localization of TJ proteins, basal ES proteins, and the framework protein vimentin at Sertoli cell-cell interfaces after Msi-1 knockdown were assessed 48 h after transfection. Sertoli cell nuclei were stained with DAPI. Note that considerably less beta-catenin and claudin-11 were detected, and the distributions of occludin and E-cadherin (white arrows) were changed at Sertoli cell-cell interfaces after Msi-1 knockdown. Scale bars: 20 mum.

Supportive validation

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Experimental details: FIGURE 3: An in vivo study assessing the role of Msi-1 in BTB function and spermatogenesis by RNAi intratesticular injection. Msi-1-targeting siRNA duplexes and nontargeting duplexes were administered to each testis in adult mice as a single treatment. The knockdown efficiency, BTB-associated protein expression, biotin tracer experiment, and hematoxylin-eosin (HE) staining at 3, 5, 9, and 12 d postintratesticular injection, respectively. (A) Considerably more intense Msi-1 staining was observed in the Sertoli cells from testes transfected with nontargeting control (a) versus testes transfected with Msi-1-specific siRNA duplexes (b). Scale bars: 20 mum. (B) Histogram summarizing immunoblotting results of Msi-1 and normalized against beta-tubulin. Each bar represents the mean +- SD of n = 3 experiments. *, p < 0.05. (C) Paraffin sections were used to study changes in the expression of beta-catenin (a and b) and claudin-11 (c and d) after Msi-1 knockdown in vivo. The boxed area was randomly selected. Scale bars: 20 mum. (D) The protein levels of beta-catenin and claudin-11 in nontargeting control and Msi-1 knockdown testes. beta-tubulin served as a loading control. (E) Histogram summarizing selected immunoblotting results in D and normalized against beta-tubulin. Each bar represents the mean +- SD of n = 3 experiments. *, p < 0.05. (F) We injected a biotin tracer into the testes of live anesthetized mice ( n = 3) and examined the subsequent changes in BTB integrity after siRNA d

Supportive validation

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Experimental details: Figure 6 Western blot analyses of the SHBG, TF, CLDN11 and TJP1 in the testes of wild-type (WT) and Prl7d1 transgenic ( Prl7d1 -TG) mice. ( A ) Representative western immunoblots; ( B ) The relative expression levels of the proteins were determined using densitometric analyses of the data that were normalized against the ACTB signal ( n = 6). The protein level in the control group was set to one. Each bar represents the mean +- SD. * p < 0.01 compared to the WT group.

Supportive validation

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Experimental details: Fig. 2 Phenotype and irreversible de-differentiation of Immortomouse (r) CPECs. a Primary Immortomouse (r) choroid plexus epithelial cells (p0) grown at 37 degC for 7 days showed the same staining patterns for cytokeratin (CK) and claudin-1 (Cldn-1) as pmCPECs isolated from wild-type mice. b When Immortomouse (r) CPECs were grown under permissive conditions (33 degC, 10U IFNgamma) the heterogenous de-differentiation process started in areas with low cell density, whereas CPECs kept their cuboidal shape longer in areas with high cell density. The contrast of the pictures in a and b was enhanced using Adobe Photoshop software. c Vimentin staining, rather than CK staining was observed at 33 degC. Cell death took place at 33 degC upon Ara-C addition to culture. d The irreversible loss of CPEC specific markers Cldn-1 and CK and an increasing proliferation rate of de-differentiated Immortomouse (r) CPECs was observed with increased passage. The first row is passage 2 (p2), the second row is p3, the third row is p4. e The cells failed to form confluent monolayers or display the correct expression pattern of epithelial markers upon shift to non-permissive temperature and IFNgamma withdrawal. Immortomouse (r) CPECs in e were stained after 7 days of non-permissive growth; the passage numbers (p) were E-cad/DAPI: p8, ZO1/beta-Cat/DAPI: p5, Cldn11/N-Cad/DAPI: p6, Cldn-1/CK/DAPI: p4. Scale bar in all immunofluorescent and phase contrast pictures = 100 mum. p0 primary culture, E-Cad E-cadh

Supportive validation

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Experimental details: Fig. 4 Phenotype of ECPC4 cells and primary mouse choroid plexus epithelial cells (pmCPECs). Immunofluorescence staining for CPEC specific proteins is shown in ECPC4 cells ( a ) and pmCPECs ( b ). a There is weak staining for the adhesion junction (AJ) protein E-Cadherin (E-Cad) and its cytoskeleton linker beta-catenin (beta-Cat) of ECPC4 cells and their localization is not specifically at the plasma membrane. Staining for tight junctional (TJ) claudins-1 and -11 was absent or showed a weak cytosolic pattern, respectively. The scaffolding protein ZO1 staining was disrupted. Additionally, the cell line failed to stain for the early epithelial marker cytokeratin but rather was positive for the mesenchymal intermediate filament protein vimentin. ECPC4 cells from passage 41 were stained on d4 in culture. b In contrast, the staining of pmCPECs stained on d7 in culture, revealed a proper distribution of all epithelial markers. pmCPECs. All staining was performed at least 3 times. Scale bars 50 mum. E-Cad E-cadherin, Cldn-1 Claudin 1, Cldn-11 claudin 11, CK cytokeratin, beta-Cat beta-catenin, ZO-1 zona occludens protein 1

Supportive validation

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Experimental details: Figure 5 Overexpression of DPT in the Sertoli cells reduces the expression levels of ZO-1 and claudin-11 in the testes. (A) Representative western blotting analyses of ZO-1 and claudin-11 in the control mice and the mice with DPT overexpression. (B) The relative expression levels of ZO-1 and claudin-11 were determined using densitometric analysis of the data normalized against the beta-actin from five different samples. The data are presented as the mean +- standard error of the mean ( a P

Supportive validation

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Experimental details: Figure 4 ICAM2, Src, and annexin II increase during CdCl 2 -induced testis damage. Immunoblotting experiments showing changes in the levels of several proteins (A). Proteins whose levels increased following CdCl 2 treatment are labeled as bold. Actin was used as an internal control. Histograms (B) summarizing immunoblotting results. Each data point was normalized against its corresponding actin data point and then against '0 h', which was arbitrarily set at 1. Each bar represents mean+- s.d. of n =3-6 rats. * P

Supportive validation

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Experimental details: Figure 3. Claudin-11 and Connexin 43 are disorganized in testicular dysgenesis. Confocal immunofluorescence of normal ( A ) and carcinoma in situ ( B and C ) human testis sections detecting claudin-11 (red, tight junctions, asterisks) and connexin 43 (green, gap junctions, open squares and triangles). Co-localization appears in yellow. Inserts are negative controls. (Bar = 50 um).

Supportive validation

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Experimental details: FIGURE 2 Expression of key EP-related cell-type specific proteins is reduced in the SV after cisplatin treatment. (A) Twenty four hours after cisplatin injection, SLC12A2 immunofluorescence intensity was significantly reduced in the apical and basal turns of the cochlea (two-way ANOVA, p < 0.0001; Sidak's multiple comparisons test, q = 0.0068 and q = 0.0022, respectively). (B,C) Representative SLC12A2 immunostaining of SV cross sections of control and cisplatin-treated mice. (D) Immunofluorescence staining intensity of KCNJ10 was unchanged between control and cisplatin-treated mice (two-way ANOVA, p = 0.1784). (E,F) Representative KCNJ10 immunostaining of SV cross sections of control and cisplatin-treated mice. White arrows point to representative intermediate cell nuclei. (G) Immunofluorescence staining intensity of CLDN11 was reduced in the basal turn of cisplatin-treated compared to control mice (two-way ANOVA, p = 0.0002; Sidak's multiple comparisons test q = 0.0418). (H,I) Representative CLDN11 immunostaining of SV cross sections of control and cisplatin-treated mice. Scale bars: 20 mum. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

Supportive validation

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Experimental details: Figure 4 Cul4 genes are required for male germ cell survival. ( A - D ) IF staining of CUL4A (red) and SCP3 (green) of P28 testis. While primary spermatocytes expressing both CUL4A ( A ) and SCP3 ( B ) are present in the CTRL testis, this population is completely missing in the dKO mutant testis ( C , D ). ( E - H ) IF staining of CUL4B (red) and SCP3 (green) of P28 testis. CUL4B is highly expressed in the Sertoli cells ( E , arrowheads) and round spermatids (Spd) of CTRL testis ( E , F ); whereas in the Cul4a/b Vasa dKO, CUL4B-positive Sertoli cells are the only cell type remaining in the seminiferous tubules ( G , H arrowheads). ( I - N ) IF staining of AR (red) and CTNNB1 (green) of P28 testicular sections. Wild-type testis show AR-high myoid cells ( I , arrows) and AR-low Sertoli cells ( I , arrowheads), and well organized germ cell/Sertoli cell network outlined by CTNNB1 staining ( J ). The dKO mutant testis retains myoid and Sertoli cells ( L , arrows and arrowheads, respectively), with disorganized residual CTNNB1 staining ( M ). DAPI counterstain is shown in ( K ) and ( N ). Spd, spermatids; Spct, spermatocytes; Spg, spermatogonia; Int, interstitial cells. ( O , P ) IF staining of CLDN11 (red) and SCP3 (green) of P28 testis. At this stage in the wildtype testis, tight junctions have formed apical to the spermatogonial stem cells to separate the basal and adluminal compartments ( O , arrowheads). CLDN11 was only detected in the basal-lateral membranes of dKO Sertoli ce

Supportive validation

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Experimental details: Figure 6 Ablation of Cul4b in both germ cells and Sertoli cells leads to BTB defects. ( A , B ) IF staining and ( C , D ) confocal microscopy of tight junction marker CLDN11 in CTRL and Cul4b Amh;Vasa testis. The insets in A and B are magnified views of boxed areas. Basement membrane outlined by dashed lines in insets. ( E , F ) IF staining of pS6 (S235/236) showing its accumulation in the mutant tubules. ( G , H ) Confocal IF of pS6 (S235/236) (red) and SCP3 (green) showing localization of pS6 (S235/236) in CTRL spermatogonia ( G , arrows), and ectopic activation in the mutant Sertoli cells ( H , arrowheads). ( I , J ) IF staining of pS6 (S240/244) showing its accumulation in the mutant tubules. ( K , L ) Confocal IF of pS6(S240/244) (red) and SCP3 (green) showing its normal expression in spermatogonia ( K , arrows) and ectopic activation in the mutant germ cells ( L , arrowheads). ( M , N ) IF of alpha-catenin (CTNNA1) showing its accumulation in the mutant testis. S, spermatogonia; P, pachytene spermatocytes; Z, zygotene spermatocytes; Spg,. White dashed lines outline the seminiferous tubules. Scale bars: 200 um in ( A , B ), ( E , F ), ( I , J ); 50 um in the rest.

Supportive validation

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Experimental details: Figure 6 Expression of CX43 and CLDN11 in prepubertal human testis grafts. ( A - C ) Immature CX43 expression profile in subcutaneous grafts (pre-graft control; 1-year-old). ( D - F ) Partially mature CX43 expression profile in intratesticular grafts (pre-graft control; 14-year-old). ( G - I ) Immature CLDN11 expression pattern in subcutaneous grafts (pre-graft control; 1-year-old). ( J ) Partially mature CLDN11 expression pattern (pre-graft control; 14-year-old). ( K , L ) Immature CLDN11 expression pattern in intratesticular grafts. ( M , N ) Expression of CX43 and CLDN11 in adult human testis tissue.