Journal: bioRxiv

Article Title: Actinotrichia-independent developmental mechanisms of spiny rays facilitate the morphological diversification of Acanthomorpha fish fins

doi: 10.1101/2025.03.01.640274

Figure Lengend Snippet: a Distribution of the actinotrichia at the tips of spiny rays (left) and soft rays (right) at three stages of fin deveolpent in fixed samples; the lower pair of panels of each stage are magnified images of the yellow dashed box in the upper panels. Spiny-ray bones are outlined in orange. b, c Actinotrichia distribution and spiny- and soft-ray bone morphology in wild-type fish (panel b , n = 8) and in the actinodin1 −/− / actinodin2 +/- knockout fish (panel c , n = 6). Actinotrichia were labeled with DAFFM DA (green), and the spiny- and soft-ray bones were labeled with alizarin red (magenta). d Schematic illustration of the spiny- and soft-ray morphology in fish with a loss of actinotrichia.

Article Snippet: To observe the actinotrichia, vital staining with 5 μM of DAFFM DA (Goryo Chemical, #SK1003-01) was used.

Techniques: Knock-Out, Labeling

Journal: bioRxiv

Article Title: Actinotrichia-independent developmental mechanisms of spiny rays facilitate the morphological diversification of Acanthomorpha fish fins

doi: 10.1101/2025.03.01.640274

Figure Lengend Snippet: Sections of the second dorsal fin showing the structural organization of the soft-ray tip in larvae at DF-st4. The same TEM images are presented corresponding to the lower panels, with the soft ray (light blue), actinotrichia (magenta), and basement membrane (yellow) highlighted in different colors. The numbers of each panels (#1, #2, #3) in correspond to the numbers in yellow dashed boxes. Mes, mesenchymal.

Article Snippet: To observe the actinotrichia, vital staining with 5 μM of DAFFM DA (Goryo Chemical, #SK1003-01) was used.

Techniques: Membrane

Journal: bioRxiv

Article Title: Actinotrichia-independent developmental mechanisms of spiny rays facilitate the morphological diversification of Acanthomorpha fish fins

doi: 10.1101/2025.03.01.640274

Figure Lengend Snippet: In spiny-ray development, mesenchymal cells (green) condense at the tips of spiny-ray bones, and the layer of extracellular matrix (ECM) (yellow) surrounds mesenchymal cells. In soft-ray development, the actinotrichia (magenta) are distributed at the tips of soft-ray bones and serve as scaffolds for mesenchymal cells (green). Micro-CT scan image were used to schematically illustrate the fin bones.

Article Snippet: To observe the actinotrichia, vital staining with 5 μM of DAFFM DA (Goryo Chemical, #SK1003-01) was used.

Techniques: Micro-CT

Journal: bioRxiv

Article Title: Actinotrichia-independent developmental mechanisms of spiny rays facilitate the morphological diversification of Acanthomorpha fish fins

doi: 10.1101/2025.03.01.640274

Figure Lengend Snippet: a Schematic illustration of the obtaining the actinodin1 ( and1 ) and actinodin2 ( and2 ) knockout fish. b Actinotrichia distribution and spiny- and soft-ray bone morphology in the and1 −/− / and2 +/+ knockout fish. Actinotrichia were labeled with DAFFM DA (green), and the spiny- and soft-ray bones were labeled with alizarin red (magenta). White brackets and arrows indicate actinotrichia. c Sequences of actinodin1 −/− / actinodin2 +/+ knockout fish, showing a mutation spectrum revealed by Sanger sequencing. Sequences in blue and green indicate the PAM and the recognition sequence for the sgRNA target, respectively. a.a., amino acids.

Article Snippet: To observe the actinotrichia, vital staining with 5 μM of DAFFM DA (Goryo Chemical, #SK1003-01) was used.

Techniques: Knock-Out, Labeling, Mutagenesis, Sequencing

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: Epidermal growth factor receptor targeting IgG3 triggers complement-mediated lysis of decay-accelerating factor expressing tumor cells through the alternative pathway amplification loop.

doi: 10.4049/jimmunol.1400329

Figure Lengend Snippet: FIGURE 4. CML triggered by anti–EGFR-IgG3 negatively correlates with CD55 and CD59 expression levels. (A) Surface expression levels of CD46, CD55, and CD59 on analyzed cell lines were quantified by calibrated flow cytometry. Means 6 SEM of at least three independent experiments are presented. (B) Correlations between CD46, CD55, or CD59 and anti–EGFR-IgG3–mediated CDC were calculated for all four cell lines. CDC results at 2 mg/ml Ab concentration were taken from experiments presented in Fig. 2. (C) A431 cells were seeded into 10-cm plates and grown overnight. On the following day, cells were transfected with 50 nM control siRNA or with single siRNAs specific for CD46, CD55, CD59, or with a combination of all three mCRP-specific siRNAs for 72 h. Efficiency of siRNA-induced knockdown was analyzed by direct flow cytometry using fluorochrome-labeled, mCRP- specific Abs (CD46-Pacific blue, CD55-PE, CD59-FITC), or respective control Abs. (D–G) CDC against control siRNA or mCRP-specific, siRNA- transfected A431 cells was analyzed by 3-h [51Cr] release assays in the presence of 25% v/v human serum and anti–EGFR-IgG1 (upper panels), anti– EGFR-IgG3 (lower panels), as well as the respective control Abs at increasing concentrations. (H) Concentration-dependent binding of CD55-Ab (BRIC216, mouse IgG1) to A431 cells was analyzed by indirect immunofluorescence. Results from one representative experiment are presented. (I) CDC triggered by anti–EGFR-IgG1, anti–EGFR-IgG3, or respective control Abs (all at 66.67 nM) against A431 cells in the presence of saturating concentrations of CD55-Ab or a control Ab (both at 66.67 nM) was analyzed by 3-h [51Cr] release assays in the presence of 25% v/v human (Figure legend continues)

Article Snippet: To block complement regulatory activity of CD55, we used mouse anti-human CD55 (66.67 nM, BRIC216, mouse IgG1; Bio-Rad) blocking mAb in CDC experiments at saturating concentrations.

Techniques: Expressing, Cytometry, Concentration Assay, Transfection, Control, Knockdown, Labeling, Binding Assay

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: Epidermal growth factor receptor targeting IgG3 triggers complement-mediated lysis of decay-accelerating factor expressing tumor cells through the alternative pathway amplification loop.

doi: 10.4049/jimmunol.1400329

Figure Lengend Snippet: FIGURE 5. CD55 dampens anti–EGFR-IgG3–triggered CML and promotes C1q-dependent induction of AP amplification. BHK-EGFR+ #5 cells were transiently transfected with a control vector or a CD55 vector for 48 h. (A) Cell-surface expression of CD55 was analyzed by direct flow cytometry using PE-conjugated CD55-specific or control Abs. (B–D) The influence of CD55 overexpression on anti–EGFR-IgG3–mediated CDC was investigated by [51Cr] release assays either (B) in an Ab concentration–response curve, (C) in a time-dependent manner, or (D) in serum titration experiments. (E–H) The influence of the alternative complement pathway inhibitor CRIg (E and G), the presence of C1q in serum (F; at 66.67 nM Ab concentration; mean 6 SEM of triplicates), as well as of factor B (H; 13.33 nM Ab concentration, 12.5% v/v factor B–depleted serum, 200 mg/ml factor B), on anti–EGFR-IgG3–mediated CDC was analyzed using either (E and F) control vector–transfected or CD55 vector–transfected BHK-EGFR+ #5 cells or (G and H) DiFi cells (66.67 nM Ab concentration). (I) Deposition of factor Bb on control vector– or CD55 vector–transfected BHK-EGFR+ #5 cells was analyzed by flow cytometry. Relative deposition levels were calculated by equating RFI measured in the absence of Ab with 100%. Results are presented as mean 6 SEM of at least three independent experiments with different blood donors. *p # 0.05 anti–EGFR-IgG3 versus respective control Ab; (B–D, I) #p # 0.05 control vector versus CD55 vector; (E and G) #p # 0.05 without CRIg-Fc versus CRIg-Fc; (H) #p # 0.05 w/o factor B versus with factor B.

Article Snippet: To block complement regulatory activity of CD55, we used mouse anti-human CD55 (66.67 nM, BRIC216, mouse IgG1; Bio-Rad) blocking mAb in CDC experiments at saturating concentrations.

Techniques: Transfection, Control, Plasmid Preparation, Expressing, Cytometry, Over Expression, Concentration Assay, Titration

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: Epidermal growth factor receptor targeting IgG3 triggers complement-mediated lysis of decay-accelerating factor expressing tumor cells through the alternative pathway amplification loop.

doi: 10.4049/jimmunol.1400329

Figure Lengend Snippet: FIGURE 6. Overview of complement activation by human anti–EGFR-IgG3 in the context of CD55 expression. On CD55-deficient target cells (left panel), anti–EGFR-IgG3 mediates strong C3b but low C4b deposition and induces assembly of classical and alternative C3 convertases, predominantly resulting in the induction of fast and efficient CDC via the classical pathway of complement activation. In contrast, on CD55-expressing target cells (right panel), CD55 mainly accelerates the decay of low amounts of classical C3 convertases, leading to amplification of the AP and finally to slow and inefficient CDC induction.

Article Snippet: To block complement regulatory activity of CD55, we used mouse anti-human CD55 (66.67 nM, BRIC216, mouse IgG1; Bio-Rad) blocking mAb in CDC experiments at saturating concentrations.

Techniques: Activation Assay, Expressing

Journal: Nutrients

Article Title: Does Vitamin K2 Influence the Interplay between Diabetes Mellitus and Intervertebral Disc Degeneration in a Rat Model?

doi: 10.3390/nu15132872

Figure Lengend Snippet: Rat-specific primers used for RTD PCR in this study.

Article Snippet: Cd55 , Decay accelerating factor , Rn00709472_m1 , 92 , 1.94 , NM_022269.2.

Techniques: Amplification

Journal: Nutrients

Article Title: Does Vitamin K2 Influence the Interplay between Diabetes Mellitus and Intervertebral Disc Degeneration in a Rat Model?

doi: 10.3390/nu15132872

Figure Lengend Snippet: Mean normalized gene expression of collagen type 1 ( Col1a1 , alpha chain, ( A )), type 2 ( Col2a1 , alpha chain ( B )), aggrecan ( Acan, ( C )), Cd55 ( D ), Cd59 ( E ), heme oxygenase (Hmox ) -1 ( F ) and suppressor of cytokine signaling ( Socs ) 3 ( G ) are shown in intervertebral disc (IVD) cells of non-diabetic (fa/+) and diabetic (fa/fa) ZDF rats fed without (wo vit.K2) and with (w vit.K2) additional vitamin K2. Outlier test: ROUT (Q = 1%). One-way ANOVA. Tukey post hoc test.

Article Snippet: Cd55 , Decay accelerating factor , Rn00709472_m1 , 92 , 1.94 , NM_022269.2.

Techniques: Gene Expression

Journal: Molecular Therapy Oncology

Article Title: Oncolytic virus V937 in combination with PD-1 blockade therapy to target immunologically quiescent liver and colorectal cancer

doi: 10.1016/j.omton.2024.200807

Figure Lengend Snippet: List of primer assay used for RNA expression analysis

Article Snippet: CD55 , Hs00167090_m1 , MAPK3 , Hs00946872_m1.

Techniques: RNA Expression

Journal: Journal of Neuroinflammation

Article Title: Complement components are upregulated and correlate with disease progression in the TDP-43 Q331K mouse model of amyotrophic lateral sclerosis

doi: 10.1186/s12974-018-1217-2

Figure Lengend Snippet: Dysregulation of complement components in the lumbar spinal cord of TDP-43 Q331K mice at three different ages of disease progression. a – f The mRNA expression profiles of the following complement components: C1qB ( a , classical pathway), C4 ( b , classical/lectin pathway), fB ( c , alternative pathway), C3 ( d , central component), CD55 ( e , regulator) and CD59a ( f , regulator) in the lumbar spinal cord of TDP-43 Q331K mice (blue bars) relative to non-transgenic (NTg, orange bars) and TDP-43 WT (green bars) mice during 3, 10 and 16 months of age. Data are expressed as means ± SEM ( n = 5 mice/group, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001, one-way ANOVA with Tukey’s post hoc test)

Article Snippet: Commercially available gene-specific Taqman probes for complement component 1, q subcomponent, beta polypeptide (C1qB; Mm01179619_m1), complement component 4 (C4; Mm00437893_g1), complement factor B (Cfb; Mm00433909_m1), complement component 3 (C3; Mm01232779_m1), CD55 antigen (Cd55; Mm00438377_m1), CD59a antigen (Cd59a; Mm00483149_m1) and complement component 5a receptor 1 (C5ar1; Mm00500292_s1) were used to amplify target gene of interest (Applied Biosystems, MA, USA).

Techniques: Biomarker Discovery, Expressing, Transgenic Assay

Journal: Journal of Neuroinflammation

Article Title: Complement components are upregulated and correlate with disease progression in the TDP-43 Q331K mouse model of amyotrophic lateral sclerosis

doi: 10.1186/s12974-018-1217-2

Figure Lengend Snippet: Dysregulation of complement components in tibialis anterior muscle of TDP-43 Q331K mice at three different ages of disease progression. a – f The mRNA expression profiles of the following complement components: C1qB ( a , classical pathway), C4 ( b , classical/lectin pathway), fB ( c , alternative pathway), C3 ( d , central component), CD55 ( e , regulator) and CD59a ( f , regulator) in tibialis anterior muscle of TDP-43 Q331K mice (blue bars) relative to non-transgenic (NTg, orange bars) and TDP-43 WT (green bars) mice during 3, 10 and 16 months of age. g The protein expression of C5a in the tibialis anterior muscle of NTg (orange bars), TDP-43 WT (green bars) and TDP-43 Q331K (blue bars) mice at 16 months. h mRNA expression of C5aR1 in the tibialis anterior muscle of TDP-43 Q331K mice relative to age-matched NTg and TDP-43 WT mice at three different ages. Data are expressed as means ± SEM ( n = 5 mice/group, * P < 0.05, ** P < 0.01, *** P < 0.001, one-way ANOVA with Tukey’s post hoc test for each age)

Article Snippet: Commercially available gene-specific Taqman probes for complement component 1, q subcomponent, beta polypeptide (C1qB; Mm01179619_m1), complement component 4 (C4; Mm00437893_g1), complement factor B (Cfb; Mm00433909_m1), complement component 3 (C3; Mm01232779_m1), CD55 antigen (Cd55; Mm00438377_m1), CD59a antigen (Cd59a; Mm00483149_m1) and complement component 5a receptor 1 (C5ar1; Mm00500292_s1) were used to amplify target gene of interest (Applied Biosystems, MA, USA).

Techniques: Biomarker Discovery, Expressing, Transgenic Assay