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Jackson Laboratory cd40 ko mice

TAC caused similar left ventricular hypertrophy, fibrosis and accumulation of immune cells in WT and <t>CD40</t> KO mice. Post-TAC survival analysis of WT (n = 41) and CD40 KO (n = 37) mice (A). The ratios of LV and LA weight to tibial length of WT and CD40 KO mice under control or TAC condition (n = 9-13), Sham indicates no actual TAC (B, C). Representative images and summary data for LV myocyte cross-sectional area determined by FITC-conjugated wheat germ agglutinin (WGA) staining (n = 5-7) (D). Representative images and quantitative data of LV fibrosis by Sirius red/Fast green staining (n = 4-7) (E). CD45 immunostaining (red) and quantitative data of LV leukocyte infiltration (n = 5-6) (F). Survival rate was analyzed by Kaplan-Meier method and compared by log-rank test. All quantitative data are reported as means ± SEM. Data were analyzed using one-way ANOVA followed by Bonferroni post hoc analysis. ns indicates nonsignificant ( p > 0.05),∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001,∗∗∗∗ p < 0.0001.

Cd40 Ko Mice, supplied by Jackson Laboratory, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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cd40 ko mice - by Bioz Stars, 2026-11

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1) Product Images from "Systolic pressure overload caused pulmonary oxidative stress, vessel remodeling and severe microvascular thrombosis in CD40 knockout mice through promoting platelet aggregation"

Article Title: Systolic pressure overload caused pulmonary oxidative stress, vessel remodeling and severe microvascular thrombosis in CD40 knockout mice through promoting platelet aggregation

Journal: Redox Biology

doi: 10.1016/j.redox.2026.104122

TAC caused similar left ventricular hypertrophy, fibrosis and accumulation of immune cells in WT and CD40 KO mice. Post-TAC survival analysis of WT (n = 41) and CD40 KO (n = 37) mice (A). The ratios of LV and LA weight to tibial length of WT and CD40 KO mice under control or TAC condition (n = 9-13), Sham indicates no actual TAC (B, C). Representative images and summary data for LV myocyte cross-sectional area determined by FITC-conjugated wheat germ agglutinin (WGA) staining (n = 5-7) (D). Representative images and quantitative data of LV fibrosis by Sirius red/Fast green staining (n = 4-7) (E). CD45 immunostaining (red) and quantitative data of LV leukocyte infiltration (n = 5-6) (F). Survival rate was analyzed by Kaplan-Meier method and compared by log-rank test. All quantitative data are reported as means ± SEM. Data were analyzed using one-way ANOVA followed by Bonferroni post hoc analysis. ns indicates nonsignificant ( p > 0.05),∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001,∗∗∗∗ p < 0.0001.

Figure Legend Snippet: TAC caused similar left ventricular hypertrophy, fibrosis and accumulation of immune cells in WT and CD40 KO mice. Post-TAC survival analysis of WT (n = 41) and CD40 KO (n = 37) mice (A). The ratios of LV and LA weight to tibial length of WT and CD40 KO mice under control or TAC condition (n = 9-13), Sham indicates no actual TAC (B, C). Representative images and summary data for LV myocyte cross-sectional area determined by FITC-conjugated wheat germ agglutinin (WGA) staining (n = 5-7) (D). Representative images and quantitative data of LV fibrosis by Sirius red/Fast green staining (n = 4-7) (E). CD45 immunostaining (red) and quantitative data of LV leukocyte infiltration (n = 5-6) (F). Survival rate was analyzed by Kaplan-Meier method and compared by log-rank test. All quantitative data are reported as means ± SEM. Data were analyzed using one-way ANOVA followed by Bonferroni post hoc analysis. ns indicates nonsignificant ( p > 0.05),∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001,∗∗∗∗ p < 0.0001.

Techniques Used: Control, Staining, Immunostaining

$TAC caused comparable LV dysfunction in WT and CD40 KO mice. Representative echocardiograms of each group (A). Summary data for LV ejection fraction (EF%), fractional shortening (FS%), LV end-diastolic and end-systolic diameter (LV-EDD, LV-ESD) and heart rate (n = 9-13) in each group (B–F). LV pressure of WT (n = 5) and CD40 KO (n = 5) mice were measured at 8 weeks after TAC, representative invasive pressure curve(G) with quantifications of end-systolic pressure (ESP)(I) and end-diastolic pressure (EDP)(J). Representative dp/dt curve(H) with quantifications of dp/dtmax (maximal rate of change in systolic pressure over time) (L) and dp/dtmin (minimal rate of change in pressure over time) (M). The rate-pressure product (K) was calculated by multiplying the heart rate by the LV end-systolic pressure. Western blot of β-MHC and vinculin (loading control, n = 3-4) (N, O). All quantitative data are reported as mean ± SEM. The statistical significance was assessed using two-tailed Student's unpaired t tests(I-M). Data were analyzed using one-way ANOVA followed by Bonferroni post hoc analysis (B–F, N, O). ns indicates nonsignificant ( p > 0.05),∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001,∗∗∗∗ p < 0.0001.$
Figure Legend Snippet: TAC caused comparable LV dysfunction in WT and CD40 KO mice. Representative echocardiograms of each group (A). Summary data for LV ejection fraction (EF%), fractional shortening (FS%), LV end-diastolic and end-systolic diameter (LV-EDD, LV-ESD) and heart rate (n = 9-13) in each group (B–F). LV pressure of WT (n = 5) and CD40 KO (n = 5) mice were measured at 8 weeks after TAC, representative invasive pressure curve(G) with quantifications of end-systolic pressure (ESP)(I) and end-diastolic pressure (EDP)(J). Representative dp/dt curve(H) with quantifications of dp/dtmax (maximal rate of change in systolic pressure over time) (L) and dp/dtmin (minimal rate of change in pressure over time) (M). The rate-pressure product (K) was calculated by multiplying the heart rate by the LV end-systolic pressure. Western blot of β-MHC and vinculin (loading control, n = 3-4) (N, O). All quantitative data are reported as mean ± SEM. The statistical significance was assessed using two-tailed Student's unpaired t tests(I-M). Data were analyzed using one-way ANOVA followed by Bonferroni post hoc analysis (B–F, N, O). ns indicates nonsignificant ( p > 0.05),∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001,∗∗∗∗ p < 0.0001.

Techniques Used: Western Blot, Control, Two Tailed Test

CD40 KO aggravated TAC-induced increase of lung weight. The ratios of lung wet weight, lung dry weight, lung water weight to tibial length (A-C). Lung water content percentage ((lung wet weight – lung dry weight)/lung wet weight × 100%) of each group mice (n = 7-13) (D). All quantitative data are reported as mean ± SEM. Data were analyzed using one-way ANOVA followed by Bonferroni post hoc analysis. ns indicates nonsignificant ( p > 0.05),∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001,∗∗∗∗ p < 0.0001.

Figure Legend Snippet: CD40 KO aggravated TAC-induced increase of lung weight. The ratios of lung wet weight, lung dry weight, lung water weight to tibial length (A-C). Lung water content percentage ((lung wet weight – lung dry weight)/lung wet weight × 100%) of each group mice (n = 7-13) (D). All quantitative data are reported as mean ± SEM. Data were analyzed using one-way ANOVA followed by Bonferroni post hoc analysis. ns indicates nonsignificant ( p > 0.05),∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001,∗∗∗∗ p < 0.0001.

Techniques Used:

CD40 KO caused robust pulmonary microvascular thrombosis in mice after TAC. Representative images of hematoxylin and eosin (HE) staining of lung tissues from the experimental groups(A) . Representative immunostaining images of Carstairs staining of the lung (Fibrin: bright red, platelets: gray blue or navy, collagen: bright blue), CD42c, CD61 and vWF in the lung (B-E). Quantitative data of CD42c immunofluorescence staining in the lung (n = 5-7) (F). The platelet counts in each group of mice (n = 8-14) (G). Mean platelet volume (n = 8-14) (H). Quantitative data of vWF in the lung (n = 5-6) (I). The CD42c and vWF staining were expressed as a percentage of positive staining area to the total area. All quantitative data are reported as mean ± SEM. Data were analyzed using one-way ANOVA followed by Bonferroni post hoc analysis. ns indicates nonsignificant ( p > 0.05),∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001,∗∗∗∗ p < 0.0001.

Figure Legend Snippet: CD40 KO caused robust pulmonary microvascular thrombosis in mice after TAC. Representative images of hematoxylin and eosin (HE) staining of lung tissues from the experimental groups(A) . Representative immunostaining images of Carstairs staining of the lung (Fibrin: bright red, platelets: gray blue or navy, collagen: bright blue), CD42c, CD61 and vWF in the lung (B-E). Quantitative data of CD42c immunofluorescence staining in the lung (n = 5-7) (F). The platelet counts in each group of mice (n = 8-14) (G). Mean platelet volume (n = 8-14) (H). Quantitative data of vWF in the lung (n = 5-6) (I). The CD42c and vWF staining were expressed as a percentage of positive staining area to the total area. All quantitative data are reported as mean ± SEM. Data were analyzed using one-way ANOVA followed by Bonferroni post hoc analysis. ns indicates nonsignificant ( p > 0.05),∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001,∗∗∗∗ p < 0.0001.

Techniques Used: Staining, Immunostaining, Immunofluorescence

CD40 KO exacerbated platelet aggregation and blood clot retraction in mice after TAC. The aggregation levels of WT and CD40 KO mouse platelets in response to 1.2 μg/ml collagen stimulation (n = 3-5) (A). The aggregation levels of WT and CD40 KO mouse platelets in response to 0.067U/ml thrombin stimulation (n = 5-6) (B). The aggregation levels of WT and CD40 KO mouse platelets in response to 3.4U/ml ADP stimulation (n = 4-5) (C). Clot retraction of WT and CD40 KO mouse platelets (n = 5-7) (D). All quantitative data are reported as mean ± SEM. Data were analyzed using one-way ANOVA followed by Bonferroni post hoc analysis. ns indicates nonsignificant ( p > 0.05),∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001,∗∗∗∗ p < 0.0001.

Figure Legend Snippet: CD40 KO exacerbated platelet aggregation and blood clot retraction in mice after TAC. The aggregation levels of WT and CD40 KO mouse platelets in response to 1.2 μg/ml collagen stimulation (n = 3-5) (A). The aggregation levels of WT and CD40 KO mouse platelets in response to 0.067U/ml thrombin stimulation (n = 5-6) (B). The aggregation levels of WT and CD40 KO mouse platelets in response to 3.4U/ml ADP stimulation (n = 4-5) (C). Clot retraction of WT and CD40 KO mouse platelets (n = 5-7) (D). All quantitative data are reported as mean ± SEM. Data were analyzed using one-way ANOVA followed by Bonferroni post hoc analysis. ns indicates nonsignificant ( p > 0.05),∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001,∗∗∗∗ p < 0.0001.

Techniques Used:

CD40 KO aggravated TAC-induced pulmonary leukocyte infiltration. Representative images and quantitative data of CD45 + cells, Mac2 + cells and CD3 + cells in lungs (n = 5-7) (A-C). All quantitative data are reported as mean ± SEM. Data were analyzed using one-way ANOVA followed by Bonferroni post hoc analysis. ns indicates nonsignificant ( p > 0.05),∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001,∗∗∗∗ p < 0.0001.

Figure Legend Snippet: CD40 KO aggravated TAC-induced pulmonary leukocyte infiltration. Representative images and quantitative data of CD45 + cells, Mac2 + cells and CD3 + cells in lungs (n = 5-7) (A-C). All quantitative data are reported as mean ± SEM. Data were analyzed using one-way ANOVA followed by Bonferroni post hoc analysis. ns indicates nonsignificant ( p > 0.05),∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001,∗∗∗∗ p < 0.0001.

Techniques Used:

CD40 KO exacerbated pulmonary fibrosis and vessel remodeling in mice after TAC. Representative images (A-C) and quantitative data (D-F) of Masson's trichrome staining and smooth muscle α-actin (red) of the lung tissues. Quantitative RT-PCR result of pulmonary TGFβ (normalized to 18S) (G). All quantitative data are reported as mean ± SEM. Data were analyzed using one-way ANOVA followed by Bonferroni post hoc analysis. ns indicates nonsignificant ( p > 0.05),∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001,∗∗∗∗ p < 0.0001.

Figure Legend Snippet: CD40 KO exacerbated pulmonary fibrosis and vessel remodeling in mice after TAC. Representative images (A-C) and quantitative data (D-F) of Masson's trichrome staining and smooth muscle α-actin (red) of the lung tissues. Quantitative RT-PCR result of pulmonary TGFβ (normalized to 18S) (G). All quantitative data are reported as mean ± SEM. Data were analyzed using one-way ANOVA followed by Bonferroni post hoc analysis. ns indicates nonsignificant ( p > 0.05),∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001,∗∗∗∗ p < 0.0001.

Techniques Used: Staining, Quantitative RT-PCR

CD40 KO exacerbated pulmonary oxidative stress in mice with existing LV dysfunction. Representative images and Quantitative data of pulmonary dihydroethidium (DHE) staining in mice (n = 5) (A, D), IHC analysis of 3′-nitrotyrosine (B, E) and 4-hydroxynonenal (n = 4-6) (C, F). All quantitative data are reported as mean ± SEM. Data were analyzed using one-way ANOVA followed by Bonferroni post hoc analysis. ns indicates nonsignificant ( p > 0.05),∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001,∗∗∗∗ p < 0.0001.

Figure Legend Snippet: CD40 KO exacerbated pulmonary oxidative stress in mice with existing LV dysfunction. Representative images and Quantitative data of pulmonary dihydroethidium (DHE) staining in mice (n = 5) (A, D), IHC analysis of 3′-nitrotyrosine (B, E) and 4-hydroxynonenal (n = 4-6) (C, F). All quantitative data are reported as mean ± SEM. Data were analyzed using one-way ANOVA followed by Bonferroni post hoc analysis. ns indicates nonsignificant ( p > 0.05),∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001,∗∗∗∗ p < 0.0001.

Techniques Used: Staining

TAC resulted in significant RV inflammation, fibrosis and cardiomyocyte hypertrophy in CD40 KO mice. The ratio of RV weight to tibial length of WT and CD40 KO mice under control or TAC condition (n = 9-13) (A). Western blot of β-MHC and loading control of vinculin (n = 3-4) (B, C)). Representative images and summary data for RV myocyte cross-sectional area determined by FITC-conjugated WGA staining (n = 6) (D). Representative images and quantitative data of RV fibrosis by Sirius red/Fast green staining (n = 5-6) (E). CD45 immunostaining (red) and quantitative data of RV leukocyte infiltration (n = 5-7) (F). All quantitative data are reported as mean ± SEM. Data were analyzed using one-way ANOVA followed by Bonferroni post hoc analysis. ns indicates nonsignificant ( p > 0.05),∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001,∗∗∗∗ p < 0.0001.

Figure Legend Snippet: TAC resulted in significant RV inflammation, fibrosis and cardiomyocyte hypertrophy in CD40 KO mice. The ratio of RV weight to tibial length of WT and CD40 KO mice under control or TAC condition (n = 9-13) (A). Western blot of β-MHC and loading control of vinculin (n = 3-4) (B, C)). Representative images and summary data for RV myocyte cross-sectional area determined by FITC-conjugated WGA staining (n = 6) (D). Representative images and quantitative data of RV fibrosis by Sirius red/Fast green staining (n = 5-6) (E). CD45 immunostaining (red) and quantitative data of RV leukocyte infiltration (n = 5-7) (F). All quantitative data are reported as mean ± SEM. Data were analyzed using one-way ANOVA followed by Bonferroni post hoc analysis. ns indicates nonsignificant ( p > 0.05),∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001,∗∗∗∗ p < 0.0001.

Techniques Used: Control, Western Blot, Staining, Immunostaining

other:

Article Title: Systolic pressure overload caused pulmonary oxidative stress, vessel remodeling and severe microvascular thrombosis in CD40 knockout mice through promoting platelet aggregation
Article Snippet: Animals and experimental design: CD40 KO mice (B6.129P2– Cd40 tm1Kik /J; stock NO: 002928) and wild type (WT) C57BL/6J mice were purchased from Jackson Laboratory and Shanghai SLAC Laboratory Animal Co, Ltd. Based on the information provided by Jackson Laboratory, CD40 KO strain has been backcrossed to C57BL/6J mice for at least 10 generations.

Article Title: Systolic pressure overload caused pulmonary oxidative stress, vessel remodeling and severe microvascular thrombosis in CD40 knockout mice through promoting platelet aggregation.
Article Snippet: Animals and experimental design: CD40 KO mice (B6.129P2–Cd40tm1Kik/J; stock NO: 002928) and wild type (WT) C57BL/6J mice were purchased from Jackson Laboratory and Shanghai SLAC Laboratory Animal Co, Ltd. Based on the information provided by Jackson Laboratory, CD40 KO strain has been backcrossed to C57BL/6J mice for at least 10 generations.

Article Title: Positioning and reversible suppression of CCR7 + dendritic cells in perivascular tumor niches shape cancer immunity
Article Snippet: WT (C57BL6/J; Cat #000664), CD45.1 (JAX #002014) were purchased from Charles River Laboratories.

Knock-In:

Article Title: Positioning and reversible suppression of CCR7 + dendritic cells in perivascular tumor niches shape cancer immunity.
Article Snippet: WT (C57BL6/J; Cat #000664), CD45.1 (JAX #002014) were purchased from Charles River Laboratories. .. Cd40-KO (JAX #002927), Il-12p40-IRES-eYFP (JAX #006412), FoxP3-IRES-mRFP (JAX #008374), Ccr7-GFP knockin/knockout (referred to as Ccr7 gfp/wt or Ccr7 ko/wt ; JAX #027913) and FoxP3-iDtr-GFP (JAX #016958) were purchased from Jackson Laboratories. ..

Knock-Out:

Article Title: CD40 controls CXCR5-induced recruitment of myeloid-derived suppressor cells to gastric cancer.
Article Snippet: Wild type C57BL/6 mice (WT; six to eight weeks old) were purchased from the Shanghai Laboratory Animal Center (Shanghai, China). .. Syngenic agematched CD40 knockout mice (KO) were purchased from the Jackson Laboratory (Maine, USA). ..

Image Search Results

(A) Schematic representation of the E. coli display system used for selections. The surface-expressed fusion protein consists of an albumin-binding domain for expression normalization and an affibody library member. Cells displaying affibody variants capable of binding biotinylated CD40L were isolated by fluorescent-activated cell sorting (FACS). The gate used for sorting is indicated in green. The x-axis shows fluorescence intensity corresponding to surface display (561/543–627 nm), and the y-axis shows fluorescence intensity corresponding to hCD40L binding (638/650–670 nm). (B) The protein structure of an affibody molecule with diversified positions indicated in yellow. (C) Flow cytometry dot plots from analysis of the naive library and the output libraries from successive selection rounds, comprising three rounds of MACS, followed by three rounds of FACS. Each plot represents one library, with axes corresponding to surface display (x-axis) and hCD40L binding (y-axis)

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Trimerization of CD40L-specific affibody molecules using collagen domains enhances target binding and CD40 blockade

doi: 10.1007/s00018-026-06301-2

Figure Lengend Snippet: (A) Schematic representation of the E. coli display system used for selections. The surface-expressed fusion protein consists of an albumin-binding domain for expression normalization and an affibody library member. Cells displaying affibody variants capable of binding biotinylated CD40L were isolated by fluorescent-activated cell sorting (FACS). The gate used for sorting is indicated in green. The x-axis shows fluorescence intensity corresponding to surface display (561/543–627 nm), and the y-axis shows fluorescence intensity corresponding to hCD40L binding (638/650–670 nm). (B) The protein structure of an affibody molecule with diversified positions indicated in yellow. (C) Flow cytometry dot plots from analysis of the naive library and the output libraries from successive selection rounds, comprising three rounds of MACS, followed by three rounds of FACS. Each plot represents one library, with axes corresponding to surface display (x-axis) and hCD40L binding (y-axis)

Article Snippet: HEK-BlueTM CD40L cells (cat.no. hkb-cd40, Invivogen) were grown according to manufacturer’s recommendations.

Techniques: Binding Assay, Expressing, Isolation, FACS, Fluorescence, Flow Cytometry, Selection

(A) Representative flow cytometry dot plots from high-throughput screening of unique affibody clones in the E. coli display format. Each dot plot corresponds to a unique clone, with axes representing surface display (x-axis) and hCD40L binding (y-axis) as described above. (B) SPR sensorgrams from soluble protein candidates, indicating their different abilities to bind to recombinant hCD40L immobilized on the chip surface. (C) Flow cytometry analysis showing binding of candidate or control affibodies and an anti-CD40L antibody to CD3 + CD4 + T cells from human peripheral blood following in vitro stimulation with phorbol myristate acetate (PMA) and ionomycin

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Trimerization of CD40L-specific affibody molecules using collagen domains enhances target binding and CD40 blockade

doi: 10.1007/s00018-026-06301-2

Figure Lengend Snippet: (A) Representative flow cytometry dot plots from high-throughput screening of unique affibody clones in the E. coli display format. Each dot plot corresponds to a unique clone, with axes representing surface display (x-axis) and hCD40L binding (y-axis) as described above. (B) SPR sensorgrams from soluble protein candidates, indicating their different abilities to bind to recombinant hCD40L immobilized on the chip surface. (C) Flow cytometry analysis showing binding of candidate or control affibodies and an anti-CD40L antibody to CD3 + CD4 + T cells from human peripheral blood following in vitro stimulation with phorbol myristate acetate (PMA) and ionomycin

Article Snippet: HEK-BlueTM CD40L cells (cat.no. hkb-cd40, Invivogen) were grown according to manufacturer’s recommendations.

Techniques: Flow Cytometry, High Throughput Screening Assay, Clone Assay, Binding Assay, Recombinant, Control, In Vitro

Biophysical characterization and binding kinetics of monomeric CD40L-binding affibody candidates. (A) Circular dichroism (CD) spectra of the affibody candidates D10 and G6 recorded at room temperature before (solid lines) and after (dashed red lines) variable temperature measurements (VTM). (B) Melting curves from the VTMs of D10 (blue) and G6 (orange) with indicated melting temperatures. (C) Sensorgrams from kinetic assessment of D10 and G6 with recombinant hCD40L immobilized on the chip surface. The respective kinetic constants are shown in the bottom table with values representing four independent measurements

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Trimerization of CD40L-specific affibody molecules using collagen domains enhances target binding and CD40 blockade

doi: 10.1007/s00018-026-06301-2

Figure Lengend Snippet: Biophysical characterization and binding kinetics of monomeric CD40L-binding affibody candidates. (A) Circular dichroism (CD) spectra of the affibody candidates D10 and G6 recorded at room temperature before (solid lines) and after (dashed red lines) variable temperature measurements (VTM). (B) Melting curves from the VTMs of D10 (blue) and G6 (orange) with indicated melting temperatures. (C) Sensorgrams from kinetic assessment of D10 and G6 with recombinant hCD40L immobilized on the chip surface. The respective kinetic constants are shown in the bottom table with values representing four independent measurements

Article Snippet: HEK-BlueTM CD40L cells (cat.no. hkb-cd40, Invivogen) were grown according to manufacturer’s recommendations.

Techniques: Binding Assay, Circular Dichroism, Recombinant

(A) Crystal structures of the NC1 domain from human collagen XV (3N3f.pdb) and human collagen XVIII (3HON.pdb) . Their respective structures are highly similar, as illustrated by the superimposition of their monomers to the right. (B) Suggested interaction geometry of hCD40L (beige) and the fusion protein candidate colXVIII-D10 (pink), superimposed with a co-crystal structure of human CD40 (green) and CD40L (3QD6.pdb) to the right. (C) Construct design for fusion proteins with NC1 domains. H 6 denotes a hexahistidine tag, Z an affibody molecule, (G 4 S) 4 the glycine-serine spacer, and colXV and colXVIII the respective NC1 domains. (D) Chromatograms from analytical SEC of indicated fusion protein candidates or controls harboring the NC1 domain in the N-terminal (left) and C-terminal (right). Z-ABD was used as an arbitrary monomer of similar molecular size to a monomeric fusion protein candidate

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Trimerization of CD40L-specific affibody molecules using collagen domains enhances target binding and CD40 blockade

doi: 10.1007/s00018-026-06301-2

Figure Lengend Snippet: (A) Crystal structures of the NC1 domain from human collagen XV (3N3f.pdb) and human collagen XVIII (3HON.pdb) . Their respective structures are highly similar, as illustrated by the superimposition of their monomers to the right. (B) Suggested interaction geometry of hCD40L (beige) and the fusion protein candidate colXVIII-D10 (pink), superimposed with a co-crystal structure of human CD40 (green) and CD40L (3QD6.pdb) to the right. (C) Construct design for fusion proteins with NC1 domains. H 6 denotes a hexahistidine tag, Z an affibody molecule, (G 4 S) 4 the glycine-serine spacer, and colXV and colXVIII the respective NC1 domains. (D) Chromatograms from analytical SEC of indicated fusion protein candidates or controls harboring the NC1 domain in the N-terminal (left) and C-terminal (right). Z-ABD was used as an arbitrary monomer of similar molecular size to a monomeric fusion protein candidate

Article Snippet: HEK-BlueTM CD40L cells (cat.no. hkb-cd40, Invivogen) were grown according to manufacturer’s recommendations.

Techniques: Construct

(A) Sensorgrams from the kinetic measurements of the N-terminal fusion protein candidates. The apparent kinetic constants were generated using a 1:1 Langmuir curve fitting model and are shown in the table. (B) Sensorgrams from two independent measurements of the CD40 blocking SPR assay. CD40 was immobilized on the chip surface and hCD40L, pre-incubated with the respective candidates or controls, was injected over the surface. The y-axis shows the normalized response units (RU) at equilibrium for each tested concentration of candidate, and the x-axis shows the molar ratio of candidate to CD40L

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Trimerization of CD40L-specific affibody molecules using collagen domains enhances target binding and CD40 blockade

doi: 10.1007/s00018-026-06301-2

Figure Lengend Snippet: (A) Sensorgrams from the kinetic measurements of the N-terminal fusion protein candidates. The apparent kinetic constants were generated using a 1:1 Langmuir curve fitting model and are shown in the table. (B) Sensorgrams from two independent measurements of the CD40 blocking SPR assay. CD40 was immobilized on the chip surface and hCD40L, pre-incubated with the respective candidates or controls, was injected over the surface. The y-axis shows the normalized response units (RU) at equilibrium for each tested concentration of candidate, and the x-axis shows the molar ratio of candidate to CD40L

Article Snippet: HEK-BlueTM CD40L cells (cat.no. hkb-cd40, Invivogen) were grown according to manufacturer’s recommendations.

Techniques: Generated, Blocking Assay, SPR Assay, Incubation, Injection, Concentration Assay

(A) Surface expression of CD40L, represented by the median fluorescent intensity (MFI), on Jurkat D1.1 cells and Jurkat wild-type (wt) cells following staining with a fluorescently labeled CD40L-specific monoclonal antibody. The data points represent duplicate values from two independent measurements. (B) Jurkat D1.1 cell binding (MFI) of monomeric and trimeric candidates or negative controls following labeling with the indicated concentrations. The data points represent duplicate values from three independent measurements. (C) Overlay of histograms displaying fluorescence intensity normalized to each population’s maximum signal (% of max) for the indicated candidates and negative controls at 100 nM, measured using the 638/655–665 nm laser/filter combination. (D) Inhibition curves from the NF-κB reporter assay showing CD40 blockade by monomeric D10 and colXVIII-D10, with colXVIII-Zwt included as a negative control

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Trimerization of CD40L-specific affibody molecules using collagen domains enhances target binding and CD40 blockade

doi: 10.1007/s00018-026-06301-2

Figure Lengend Snippet: (A) Surface expression of CD40L, represented by the median fluorescent intensity (MFI), on Jurkat D1.1 cells and Jurkat wild-type (wt) cells following staining with a fluorescently labeled CD40L-specific monoclonal antibody. The data points represent duplicate values from two independent measurements. (B) Jurkat D1.1 cell binding (MFI) of monomeric and trimeric candidates or negative controls following labeling with the indicated concentrations. The data points represent duplicate values from three independent measurements. (C) Overlay of histograms displaying fluorescence intensity normalized to each population’s maximum signal (% of max) for the indicated candidates and negative controls at 100 nM, measured using the 638/655–665 nm laser/filter combination. (D) Inhibition curves from the NF-κB reporter assay showing CD40 blockade by monomeric D10 and colXVIII-D10, with colXVIII-Zwt included as a negative control

Article Snippet: HEK-BlueTM CD40L cells (cat.no. hkb-cd40, Invivogen) were grown according to manufacturer’s recommendations.

Techniques: Expressing, Staining, Labeling, Binding Assay, Fluorescence, Inhibition, Reporter Assay, Negative Control

Review

cd40 ko mice (Jackson Laboratory)

Structured Review

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1) Product Images from "Systolic pressure overload caused pulmonary oxidative stress, vessel remodeling and severe microvascular thrombosis in CD40 knockout mice through promoting platelet aggregation"

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