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colon cell line ccd841  (ATCC)


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    Structured Review

    ATCC colon cell line ccd841
    Colon Cell Line Ccd841, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 640 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/colon cell line ccd841/product/ATCC
    Average 98 stars, based on 640 article reviews
    colon cell line ccd841 - by Bioz Stars, 2026-03
    98/100 stars

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    Representative fundus photographs (A–D) and FFA (E–H) of the retinas in the NC and EIU groups. (A) Fundus photograph from the WT NC group. (B) Fundus photograph from the KO NC group. (C) Fundus photograph from the WT EIU group. (D) Fundus photograph from the KO EIU group. (E) FFA from the WT NC group. (F) FFA from the KO NC group. (G) FFA from the WT EIU group. (H) FFA from the KO EIU group. (I) Grade of the severity of vitreous opacity. ∗∗ P < 0.01. n = 3 biological replicates per group. FFA, fundus <t>fluorescein</t> angiography; WT, wild type; KO, Cgas knockout; NC, normal control; EIU, endotoxin-induced uveitis.
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    Representative fundus photographs (A–D) and FFA (E–H) of the retinas in the NC and EIU groups. (A) Fundus photograph from the WT NC group. (B) Fundus photograph from the KO NC group. (C) Fundus photograph from the WT EIU group. (D) Fundus photograph from the KO EIU group. (E) FFA from the WT NC group. (F) FFA from the KO NC group. (G) FFA from the WT EIU group. (H) FFA from the KO EIU group. (I) Grade of the severity of vitreous opacity. ∗∗ P < 0.01. n = 3 biological replicates per group. FFA, fundus <t>fluorescein</t> angiography; WT, wild type; KO, Cgas knockout; NC, normal control; EIU, endotoxin-induced uveitis.
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    Representative fundus photographs (A–D) and FFA (E–H) of the retinas in the NC and EIU groups. (A) Fundus photograph from the WT NC group. (B) Fundus photograph from the KO NC group. (C) Fundus photograph from the WT EIU group. (D) Fundus photograph from the KO EIU group. (E) FFA from the WT NC group. (F) FFA from the KO NC group. (G) FFA from the WT EIU group. (H) FFA from the KO EIU group. (I) Grade of the severity of vitreous opacity. ∗∗ P < 0.01. n = 3 biological replicates per group. FFA, fundus <t>fluorescein</t> angiography; WT, wild type; KO, Cgas knockout; NC, normal control; EIU, endotoxin-induced uveitis.
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    Representative fundus photographs (A–D) and FFA (E–H) of the retinas in the NC and EIU groups. (A) Fundus photograph from the WT NC group. (B) Fundus photograph from the KO NC group. (C) Fundus photograph from the WT EIU group. (D) Fundus photograph from the KO EIU group. (E) FFA from the WT NC group. (F) FFA from the KO NC group. (G) FFA from the WT EIU group. (H) FFA from the KO EIU group. (I) Grade of the severity of vitreous opacity. ∗∗ P < 0.01. n = 3 biological replicates per group. FFA, fundus <t>fluorescein</t> angiography; WT, wild type; KO, Cgas knockout; NC, normal control; EIU, endotoxin-induced uveitis.
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    Vector Laboratories cona lectin
    a , Experimental design (created with BioRender.com ). Inhibition of PYGL-mediated glycogenolysis by CP-91149 in vivo. WT mice under a regular 12 h light–dark cycle and NR feeding were subcutaneously injected with either vehicle (Veh) or CP-91149 at ZT0 for tissue collections at ZT3, ZT6, ZT9, ZT12 and ZT24. b , Average food consumption of WT mice ( n = 4 biological replicates) 24 h after CP-91149 injection. c , Temporal profiles of glycogen in the liver of Veh-injected and CP-91149-injected mice ( n = 20 (5 timepoints × 4 biological replicates)). d , Glycosylation levels of proteins in CP-91149-treated and vehicle-treated mouse liver were determined by <t>lectin</t> blot analysis with concanavalin A <t>(ConA,</t> n = 20 (5 timepoints × 4 biological replicates)). Amido black staining of the membranes was used as a loading control and serves as a reference for normalization of the quantified values (right). e , C3 levels in mouse serum as assessed by ELISA ( n = 20 (5 timepoints × 4 biological replicates)). f , Experimental design (created with BioRender.com ). Inhibition of PYGL-mediated glycogenolysis by CP-91149 in AML12 mouse hepatocytes. Treatment with Veh or CP-91149 (67 µM) was performed for 3, 6, 12 and 24 h. g , h , Kinetic profiles of UDP-glucose + UDP-galactose levels ( g ), cytidine 5′-monophospho-N-acetyl neuraminic acid (CMP-Neu5Ac) ( h , left) and uridine diphosphate N-acetylglucosamine (UDP-GlcNAc) ( h , right) in AML12 cells upon CP-91149 treatment ( n = 16 (4 timepoints × 4 biological replicates)). i , Glycosylation levels of proteins in CP-91149-treated and vehicle-treated AML12 cells were determined by lectin blot analysis with ConA ( n = 16 (4 timepoints × 4 biological replicates)). Amido black staining of the membranes was used as a loading control and serves as a reference for normalization of the quantified values (bottom). j , ALB, FN1 and C3 levels in cell medium determined by ELISA ( n = 22–24 (4 timepoints × 6 biological replicates, with ALB 14 h Veh and 24 h CP-91149 n = 5)). k , Experimental design (created with BioRender.com ). AML12 cells were treated with Veh or CP-91149 for 14 h in the absence or presence of supplemental UDP-glucose (UDPG; 2 mM). l , m , ALB and C3 levels in cell medium ( l ) and lysates ( m ) as determined by ELISA ( n = 6 biological replicates, except for ALB under CP-91149 treatment ( n = 5)). Data are displayed as means; error bars, s.e.m. Boxplots show the median (centre line), interquartile range (box) and minimum to maximum values (whiskers). A detailed description of the statistical analysis is available in Source Data Fig. . See also Extended Data Fig. .
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    Image Search Results


    Representative fundus photographs (A–D) and FFA (E–H) of the retinas in the NC and EIU groups. (A) Fundus photograph from the WT NC group. (B) Fundus photograph from the KO NC group. (C) Fundus photograph from the WT EIU group. (D) Fundus photograph from the KO EIU group. (E) FFA from the WT NC group. (F) FFA from the KO NC group. (G) FFA from the WT EIU group. (H) FFA from the KO EIU group. (I) Grade of the severity of vitreous opacity. ∗∗ P < 0.01. n = 3 biological replicates per group. FFA, fundus fluorescein angiography; WT, wild type; KO, Cgas knockout; NC, normal control; EIU, endotoxin-induced uveitis.

    Journal: Genes & Diseases

    Article Title: cGAS knockout inhibited endotoxin-induced uveitis in mice

    doi: 10.1016/j.gendis.2025.101786

    Figure Lengend Snippet: Representative fundus photographs (A–D) and FFA (E–H) of the retinas in the NC and EIU groups. (A) Fundus photograph from the WT NC group. (B) Fundus photograph from the KO NC group. (C) Fundus photograph from the WT EIU group. (D) Fundus photograph from the KO EIU group. (E) FFA from the WT NC group. (F) FFA from the KO NC group. (G) FFA from the WT EIU group. (H) FFA from the KO EIU group. (I) Grade of the severity of vitreous opacity. ∗∗ P < 0.01. n = 3 biological replicates per group. FFA, fundus fluorescein angiography; WT, wild type; KO, Cgas knockout; NC, normal control; EIU, endotoxin-induced uveitis.

    Article Snippet: Concanavalin A and fluorescein (FL-1001-25; Vectorlabs) were dissolved in PBS.

    Techniques: Knock-Out, Control

    a , Experimental design (created with BioRender.com ). Inhibition of PYGL-mediated glycogenolysis by CP-91149 in vivo. WT mice under a regular 12 h light–dark cycle and NR feeding were subcutaneously injected with either vehicle (Veh) or CP-91149 at ZT0 for tissue collections at ZT3, ZT6, ZT9, ZT12 and ZT24. b , Average food consumption of WT mice ( n = 4 biological replicates) 24 h after CP-91149 injection. c , Temporal profiles of glycogen in the liver of Veh-injected and CP-91149-injected mice ( n = 20 (5 timepoints × 4 biological replicates)). d , Glycosylation levels of proteins in CP-91149-treated and vehicle-treated mouse liver were determined by lectin blot analysis with concanavalin A (ConA, n = 20 (5 timepoints × 4 biological replicates)). Amido black staining of the membranes was used as a loading control and serves as a reference for normalization of the quantified values (right). e , C3 levels in mouse serum as assessed by ELISA ( n = 20 (5 timepoints × 4 biological replicates)). f , Experimental design (created with BioRender.com ). Inhibition of PYGL-mediated glycogenolysis by CP-91149 in AML12 mouse hepatocytes. Treatment with Veh or CP-91149 (67 µM) was performed for 3, 6, 12 and 24 h. g , h , Kinetic profiles of UDP-glucose + UDP-galactose levels ( g ), cytidine 5′-monophospho-N-acetyl neuraminic acid (CMP-Neu5Ac) ( h , left) and uridine diphosphate N-acetylglucosamine (UDP-GlcNAc) ( h , right) in AML12 cells upon CP-91149 treatment ( n = 16 (4 timepoints × 4 biological replicates)). i , Glycosylation levels of proteins in CP-91149-treated and vehicle-treated AML12 cells were determined by lectin blot analysis with ConA ( n = 16 (4 timepoints × 4 biological replicates)). Amido black staining of the membranes was used as a loading control and serves as a reference for normalization of the quantified values (bottom). j , ALB, FN1 and C3 levels in cell medium determined by ELISA ( n = 22–24 (4 timepoints × 6 biological replicates, with ALB 14 h Veh and 24 h CP-91149 n = 5)). k , Experimental design (created with BioRender.com ). AML12 cells were treated with Veh or CP-91149 for 14 h in the absence or presence of supplemental UDP-glucose (UDPG; 2 mM). l , m , ALB and C3 levels in cell medium ( l ) and lysates ( m ) as determined by ELISA ( n = 6 biological replicates, except for ALB under CP-91149 treatment ( n = 5)). Data are displayed as means; error bars, s.e.m. Boxplots show the median (centre line), interquartile range (box) and minimum to maximum values (whiskers). A detailed description of the statistical analysis is available in Source Data Fig. . See also Extended Data Fig. .

    Journal: Nature Metabolism

    Article Title: Feeding-regulated glycogen metabolism drives rhythmic liver protein secretion

    doi: 10.1038/s42255-026-01453-8

    Figure Lengend Snippet: a , Experimental design (created with BioRender.com ). Inhibition of PYGL-mediated glycogenolysis by CP-91149 in vivo. WT mice under a regular 12 h light–dark cycle and NR feeding were subcutaneously injected with either vehicle (Veh) or CP-91149 at ZT0 for tissue collections at ZT3, ZT6, ZT9, ZT12 and ZT24. b , Average food consumption of WT mice ( n = 4 biological replicates) 24 h after CP-91149 injection. c , Temporal profiles of glycogen in the liver of Veh-injected and CP-91149-injected mice ( n = 20 (5 timepoints × 4 biological replicates)). d , Glycosylation levels of proteins in CP-91149-treated and vehicle-treated mouse liver were determined by lectin blot analysis with concanavalin A (ConA, n = 20 (5 timepoints × 4 biological replicates)). Amido black staining of the membranes was used as a loading control and serves as a reference for normalization of the quantified values (right). e , C3 levels in mouse serum as assessed by ELISA ( n = 20 (5 timepoints × 4 biological replicates)). f , Experimental design (created with BioRender.com ). Inhibition of PYGL-mediated glycogenolysis by CP-91149 in AML12 mouse hepatocytes. Treatment with Veh or CP-91149 (67 µM) was performed for 3, 6, 12 and 24 h. g , h , Kinetic profiles of UDP-glucose + UDP-galactose levels ( g ), cytidine 5′-monophospho-N-acetyl neuraminic acid (CMP-Neu5Ac) ( h , left) and uridine diphosphate N-acetylglucosamine (UDP-GlcNAc) ( h , right) in AML12 cells upon CP-91149 treatment ( n = 16 (4 timepoints × 4 biological replicates)). i , Glycosylation levels of proteins in CP-91149-treated and vehicle-treated AML12 cells were determined by lectin blot analysis with ConA ( n = 16 (4 timepoints × 4 biological replicates)). Amido black staining of the membranes was used as a loading control and serves as a reference for normalization of the quantified values (bottom). j , ALB, FN1 and C3 levels in cell medium determined by ELISA ( n = 22–24 (4 timepoints × 6 biological replicates, with ALB 14 h Veh and 24 h CP-91149 n = 5)). k , Experimental design (created with BioRender.com ). AML12 cells were treated with Veh or CP-91149 for 14 h in the absence or presence of supplemental UDP-glucose (UDPG; 2 mM). l , m , ALB and C3 levels in cell medium ( l ) and lysates ( m ) as determined by ELISA ( n = 6 biological replicates, except for ALB under CP-91149 treatment ( n = 5)). Data are displayed as means; error bars, s.e.m. Boxplots show the median (centre line), interquartile range (box) and minimum to maximum values (whiskers). A detailed description of the statistical analysis is available in Source Data Fig. . See also Extended Data Fig. .

    Article Snippet: Primary antibodies were used at the following dilutions: 1:1,000 for ATF4 (Cell Signaling Technologies, 11815), ARFGAP1 (Cell Signaling Technologies, 14608), Phospho-RPS6 (Cell Signaling Technologies, 2211), Total-RPS6 (Cell Signaling Technologies, 2217), GABARAPL1 (Genetex, GTX132664) and ConA Lectin (Vector Laboratories, B-1005) and 1:2,000 for STX4 (ProteinTech, 14988-1-AP).

    Techniques: Inhibition, In Vivo, Injection, Glycoproteomics, Staining, Control, Enzyme-linked Immunosorbent Assay