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gfp mouse vinculin full length  (Addgene inc)


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    Addgene inc gfp mouse vinculin full length
    Figure 1. Decreased cytoskeleton-associated <t>vinculin</t> in hindlimb muscles from Chkb-deficient mice. (A) Transmission electron microscopy of the forelimb and hindlimb from 12-d-old wild-type (Chkb+/+) and Chkb-deficient (Chkb−/−) mice shows aligned Z-bands (white arrows) and normal mitochondria (white asterisk) in hindlimb and forelimb muscle samples from wild-type and forelimb samples from Chkb−/−mice. Disrupted integrity of intercalated disk and Z-line (black arrow), mitochondrial degeneration with erased cristae (black asterisk), and prominent sarcomere degeneration in hindlimb samples from Chkb−/−mice. Scale bar = 800 nm. (B, C, D, E) Decreased cytoskeletal association of vinculin in hindlimb muscles from Chkb−/−mice compared with their wild-type littermates. (B, D) Representative micrograph of frozen hindlimb skeletal muscle tissue from wild-type and Chkb-deficient mice fixed without (B) or with (D) cytoskeleton stabilization buffer (CSK) treatment. Tissue sections were immuno-stained using anti-vinculin (purple) and Alexa Fluor 488-phalloidin (actin, green) antibody. Images were obtained using confocal microscopy. CSK treatment removes cytoplasmic proteins as well as proteins that are loosely attached to the cytoskeleton from cells but not proteins tightly binding to cytoskeleton. Thus, activated and cytoskeleton-associated vinculin can be visualized by CSK treatment. There is an increase in total vinculin
    Gfp Mouse Vinculin Full Length, supplied by Addgene inc, used in various techniques. Bioz Stars score: 91/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Defects in integrin complex formation promote CHKB -mediated muscular dystrophy."

    Article Title: Defects in integrin complex formation promote CHKB -mediated muscular dystrophy.

    Journal: Life science alliance

    doi: 10.26508/lsa.202301956

    Figure 1. Decreased cytoskeleton-associated vinculin in hindlimb muscles from Chkb-deficient mice. (A) Transmission electron microscopy of the forelimb and hindlimb from 12-d-old wild-type (Chkb+/+) and Chkb-deficient (Chkb−/−) mice shows aligned Z-bands (white arrows) and normal mitochondria (white asterisk) in hindlimb and forelimb muscle samples from wild-type and forelimb samples from Chkb−/−mice. Disrupted integrity of intercalated disk and Z-line (black arrow), mitochondrial degeneration with erased cristae (black asterisk), and prominent sarcomere degeneration in hindlimb samples from Chkb−/−mice. Scale bar = 800 nm. (B, C, D, E) Decreased cytoskeletal association of vinculin in hindlimb muscles from Chkb−/−mice compared with their wild-type littermates. (B, D) Representative micrograph of frozen hindlimb skeletal muscle tissue from wild-type and Chkb-deficient mice fixed without (B) or with (D) cytoskeleton stabilization buffer (CSK) treatment. Tissue sections were immuno-stained using anti-vinculin (purple) and Alexa Fluor 488-phalloidin (actin, green) antibody. Images were obtained using confocal microscopy. CSK treatment removes cytoplasmic proteins as well as proteins that are loosely attached to the cytoskeleton from cells but not proteins tightly binding to cytoskeleton. Thus, activated and cytoskeleton-associated vinculin can be visualized by CSK treatment. There is an increase in total vinculin
    Figure Legend Snippet: Figure 1. Decreased cytoskeleton-associated vinculin in hindlimb muscles from Chkb-deficient mice. (A) Transmission electron microscopy of the forelimb and hindlimb from 12-d-old wild-type (Chkb+/+) and Chkb-deficient (Chkb−/−) mice shows aligned Z-bands (white arrows) and normal mitochondria (white asterisk) in hindlimb and forelimb muscle samples from wild-type and forelimb samples from Chkb−/−mice. Disrupted integrity of intercalated disk and Z-line (black arrow), mitochondrial degeneration with erased cristae (black asterisk), and prominent sarcomere degeneration in hindlimb samples from Chkb−/−mice. Scale bar = 800 nm. (B, C, D, E) Decreased cytoskeletal association of vinculin in hindlimb muscles from Chkb−/−mice compared with their wild-type littermates. (B, D) Representative micrograph of frozen hindlimb skeletal muscle tissue from wild-type and Chkb-deficient mice fixed without (B) or with (D) cytoskeleton stabilization buffer (CSK) treatment. Tissue sections were immuno-stained using anti-vinculin (purple) and Alexa Fluor 488-phalloidin (actin, green) antibody. Images were obtained using confocal microscopy. CSK treatment removes cytoplasmic proteins as well as proteins that are loosely attached to the cytoskeleton from cells but not proteins tightly binding to cytoskeleton. Thus, activated and cytoskeleton-associated vinculin can be visualized by CSK treatment. There is an increase in total vinculin

    Techniques Used: Muscles, Transmission Assay, Electron Microscopy, Staining, Confocal Microscopy, Binding Assay

    Figure 3. Loss of choline kinase activity decreases the affinity of in integrin- mediated linkage component for the membrane/cytoskeleton. (A, B) Soluble (A) and insoluble (sarcolemma/cytoskeleton associated) (B) fractions prepared from hindlimb skeletal muscle (quadriceps) of three distinct (lanes 1–3) Chkb+/+ and three distinct (lanes 4–6) Chkb−/−mice probed with anti-vinculin, anti- talin, anti-α-actinin, and anti-β-actin. (C) Densitometry of the Western blot data show the ratio of detergent insoluble to detergent soluble fractions of vinculin, β-actin, and α-actinin in hindlimb (quadriceps) samples. Much less vinculin, β-actin, and α-actinin was associated with the cytoskeleton in lysates from Chkb−/−, compared with Chkb+/+ mice. Values are means ± SD; n = 3–4 per group. *P < 0.05, **P < 0.01, ***P < 0.001 (t test).
    Figure Legend Snippet: Figure 3. Loss of choline kinase activity decreases the affinity of in integrin- mediated linkage component for the membrane/cytoskeleton. (A, B) Soluble (A) and insoluble (sarcolemma/cytoskeleton associated) (B) fractions prepared from hindlimb skeletal muscle (quadriceps) of three distinct (lanes 1–3) Chkb+/+ and three distinct (lanes 4–6) Chkb−/−mice probed with anti-vinculin, anti- talin, anti-α-actinin, and anti-β-actin. (C) Densitometry of the Western blot data show the ratio of detergent insoluble to detergent soluble fractions of vinculin, β-actin, and α-actinin in hindlimb (quadriceps) samples. Much less vinculin, β-actin, and α-actinin was associated with the cytoskeleton in lysates from Chkb−/−, compared with Chkb+/+ mice. Values are means ± SD; n = 3–4 per group. *P < 0.05, **P < 0.01, ***P < 0.001 (t test).

    Techniques Used: Activity Assay, Membrane, Western Blot

    Figure 2. Decreased abundance and sarcolemma association of integrin-mediated linkage components in affected muscle of Chkb2/2 mice. (A, B) Western blot of total tissue lysis of (A) forelimb (triceps) and (B) hindlimb (quadriceps) samples from three distinct (lanes 1–3) Chkb+/+ and three distinct (lanes 4–6) Chkb−/−mice probed with anti-vinculin, anti-itga7, anti-talin, anti-α-actinin, and anti-Gapdh antibodies. Bottom: densitometry of the Western blot data show the ratio of vinculin, metavinculin, itga7, talin, and a-actinin to Gapdh in forelimb (triceps) and hindlimb (quadriceps) samples. Values are means ± SD; n = 3–4 per group. *P < 0.05, **P < 0.01, ***P < 0.001 (t test). Detergent (NP40), soluble (cytosolic).
    Figure Legend Snippet: Figure 2. Decreased abundance and sarcolemma association of integrin-mediated linkage components in affected muscle of Chkb2/2 mice. (A, B) Western blot of total tissue lysis of (A) forelimb (triceps) and (B) hindlimb (quadriceps) samples from three distinct (lanes 1–3) Chkb+/+ and three distinct (lanes 4–6) Chkb−/−mice probed with anti-vinculin, anti-itga7, anti-talin, anti-α-actinin, and anti-Gapdh antibodies. Bottom: densitometry of the Western blot data show the ratio of vinculin, metavinculin, itga7, talin, and a-actinin to Gapdh in forelimb (triceps) and hindlimb (quadriceps) samples. Values are means ± SD; n = 3–4 per group. *P < 0.05, **P < 0.01, ***P < 0.001 (t test). Detergent (NP40), soluble (cytosolic).

    Techniques Used: Western Blot, Lysis

    Figure 4. Treatment with choline kinase alpha inhibitors results in mis-localization of PI(4,5)P2 and decreases vinculin localization in focal adhesions in control U2OS cells but has no effect on U2OS cells overexpressing Myc-CHKB. (A) U2OS cells were transiently transfected with the PI(4,5)P2 reporter PH-PLCD1-GFP and were treated with the choline kinase alpha inhibitors EB-3D (10 mM), CK-37 (15 mM) or vehicle for 48 h and live cells were imaged by spinning-disk confocal microscopy. Choline kinase alpha inhibition resulted in the loss of dorsal membrane PH- PLCD1-GFP clusters in the U2OS cells. (B) The ratio of dorsal plasma membrane: cytoplasmic PH-PLCD1-GFP fluorescence is significantly decreased in choline kinase
    Figure Legend Snippet: Figure 4. Treatment with choline kinase alpha inhibitors results in mis-localization of PI(4,5)P2 and decreases vinculin localization in focal adhesions in control U2OS cells but has no effect on U2OS cells overexpressing Myc-CHKB. (A) U2OS cells were transiently transfected with the PI(4,5)P2 reporter PH-PLCD1-GFP and were treated with the choline kinase alpha inhibitors EB-3D (10 mM), CK-37 (15 mM) or vehicle for 48 h and live cells were imaged by spinning-disk confocal microscopy. Choline kinase alpha inhibition resulted in the loss of dorsal membrane PH- PLCD1-GFP clusters in the U2OS cells. (B) The ratio of dorsal plasma membrane: cytoplasmic PH-PLCD1-GFP fluorescence is significantly decreased in choline kinase

    Techniques Used: Control, Transfection, Confocal Microscopy, Inhibition, Membrane, Clinical Proteomics



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    Figure 1. Decreased cytoskeleton-associated <t>vinculin</t> in hindlimb muscles from Chkb-deficient mice. (A) Transmission electron microscopy of the forelimb and hindlimb from 12-d-old wild-type (Chkb+/+) and Chkb-deficient (Chkb−/−) mice shows aligned Z-bands (white arrows) and normal mitochondria (white asterisk) in hindlimb and forelimb muscle samples from wild-type and forelimb samples from Chkb−/−mice. Disrupted integrity of intercalated disk and Z-line (black arrow), mitochondrial degeneration with erased cristae (black asterisk), and prominent sarcomere degeneration in hindlimb samples from Chkb−/−mice. Scale bar = 800 nm. (B, C, D, E) Decreased cytoskeletal association of vinculin in hindlimb muscles from Chkb−/−mice compared with their wild-type littermates. (B, D) Representative micrograph of frozen hindlimb skeletal muscle tissue from wild-type and Chkb-deficient mice fixed without (B) or with (D) cytoskeleton stabilization buffer (CSK) treatment. Tissue sections were immuno-stained using anti-vinculin (purple) and Alexa Fluor 488-phalloidin (actin, green) antibody. Images were obtained using confocal microscopy. CSK treatment removes cytoplasmic proteins as well as proteins that are loosely attached to the cytoskeleton from cells but not proteins tightly binding to cytoskeleton. Thus, activated and cytoskeleton-associated vinculin can be visualized by CSK treatment. There is an increase in total vinculin
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    Image Search Results


    Figure 1. Decreased cytoskeleton-associated vinculin in hindlimb muscles from Chkb-deficient mice. (A) Transmission electron microscopy of the forelimb and hindlimb from 12-d-old wild-type (Chkb+/+) and Chkb-deficient (Chkb−/−) mice shows aligned Z-bands (white arrows) and normal mitochondria (white asterisk) in hindlimb and forelimb muscle samples from wild-type and forelimb samples from Chkb−/−mice. Disrupted integrity of intercalated disk and Z-line (black arrow), mitochondrial degeneration with erased cristae (black asterisk), and prominent sarcomere degeneration in hindlimb samples from Chkb−/−mice. Scale bar = 800 nm. (B, C, D, E) Decreased cytoskeletal association of vinculin in hindlimb muscles from Chkb−/−mice compared with their wild-type littermates. (B, D) Representative micrograph of frozen hindlimb skeletal muscle tissue from wild-type and Chkb-deficient mice fixed without (B) or with (D) cytoskeleton stabilization buffer (CSK) treatment. Tissue sections were immuno-stained using anti-vinculin (purple) and Alexa Fluor 488-phalloidin (actin, green) antibody. Images were obtained using confocal microscopy. CSK treatment removes cytoplasmic proteins as well as proteins that are loosely attached to the cytoskeleton from cells but not proteins tightly binding to cytoskeleton. Thus, activated and cytoskeleton-associated vinculin can be visualized by CSK treatment. There is an increase in total vinculin

    Journal: Life science alliance

    Article Title: Defects in integrin complex formation promote CHKB -mediated muscular dystrophy.

    doi: 10.26508/lsa.202301956

    Figure Lengend Snippet: Figure 1. Decreased cytoskeleton-associated vinculin in hindlimb muscles from Chkb-deficient mice. (A) Transmission electron microscopy of the forelimb and hindlimb from 12-d-old wild-type (Chkb+/+) and Chkb-deficient (Chkb−/−) mice shows aligned Z-bands (white arrows) and normal mitochondria (white asterisk) in hindlimb and forelimb muscle samples from wild-type and forelimb samples from Chkb−/−mice. Disrupted integrity of intercalated disk and Z-line (black arrow), mitochondrial degeneration with erased cristae (black asterisk), and prominent sarcomere degeneration in hindlimb samples from Chkb−/−mice. Scale bar = 800 nm. (B, C, D, E) Decreased cytoskeletal association of vinculin in hindlimb muscles from Chkb−/−mice compared with their wild-type littermates. (B, D) Representative micrograph of frozen hindlimb skeletal muscle tissue from wild-type and Chkb-deficient mice fixed without (B) or with (D) cytoskeleton stabilization buffer (CSK) treatment. Tissue sections were immuno-stained using anti-vinculin (purple) and Alexa Fluor 488-phalloidin (actin, green) antibody. Images were obtained using confocal microscopy. CSK treatment removes cytoplasmic proteins as well as proteins that are loosely attached to the cytoskeleton from cells but not proteins tightly binding to cytoskeleton. Thus, activated and cytoskeleton-associated vinculin can be visualized by CSK treatment. There is an increase in total vinculin

    Article Snippet: GFP-mouse vinculin full length (889) was a gift from Alpha Yap (plasmid #67935; Addgene; http://n2t.net/addgene:67935; RRID:Addgene_67935), mRFP-Lact-C2 was a gift from Sergio Grinstein (plasmid #74061; Addgene; http://n2t.net/addgene:74061; RRID:Addgene_74061) and was previously described (52).

    Techniques: Muscles, Transmission Assay, Electron Microscopy, Staining, Confocal Microscopy, Binding Assay

    Figure 3. Loss of choline kinase activity decreases the affinity of in integrin- mediated linkage component for the membrane/cytoskeleton. (A, B) Soluble (A) and insoluble (sarcolemma/cytoskeleton associated) (B) fractions prepared from hindlimb skeletal muscle (quadriceps) of three distinct (lanes 1–3) Chkb+/+ and three distinct (lanes 4–6) Chkb−/−mice probed with anti-vinculin, anti- talin, anti-α-actinin, and anti-β-actin. (C) Densitometry of the Western blot data show the ratio of detergent insoluble to detergent soluble fractions of vinculin, β-actin, and α-actinin in hindlimb (quadriceps) samples. Much less vinculin, β-actin, and α-actinin was associated with the cytoskeleton in lysates from Chkb−/−, compared with Chkb+/+ mice. Values are means ± SD; n = 3–4 per group. *P < 0.05, **P < 0.01, ***P < 0.001 (t test).

    Journal: Life science alliance

    Article Title: Defects in integrin complex formation promote CHKB -mediated muscular dystrophy.

    doi: 10.26508/lsa.202301956

    Figure Lengend Snippet: Figure 3. Loss of choline kinase activity decreases the affinity of in integrin- mediated linkage component for the membrane/cytoskeleton. (A, B) Soluble (A) and insoluble (sarcolemma/cytoskeleton associated) (B) fractions prepared from hindlimb skeletal muscle (quadriceps) of three distinct (lanes 1–3) Chkb+/+ and three distinct (lanes 4–6) Chkb−/−mice probed with anti-vinculin, anti- talin, anti-α-actinin, and anti-β-actin. (C) Densitometry of the Western blot data show the ratio of detergent insoluble to detergent soluble fractions of vinculin, β-actin, and α-actinin in hindlimb (quadriceps) samples. Much less vinculin, β-actin, and α-actinin was associated with the cytoskeleton in lysates from Chkb−/−, compared with Chkb+/+ mice. Values are means ± SD; n = 3–4 per group. *P < 0.05, **P < 0.01, ***P < 0.001 (t test).

    Article Snippet: GFP-mouse vinculin full length (889) was a gift from Alpha Yap (plasmid #67935; Addgene; http://n2t.net/addgene:67935; RRID:Addgene_67935), mRFP-Lact-C2 was a gift from Sergio Grinstein (plasmid #74061; Addgene; http://n2t.net/addgene:74061; RRID:Addgene_74061) and was previously described (52).

    Techniques: Activity Assay, Membrane, Western Blot

    Figure 2. Decreased abundance and sarcolemma association of integrin-mediated linkage components in affected muscle of Chkb2/2 mice. (A, B) Western blot of total tissue lysis of (A) forelimb (triceps) and (B) hindlimb (quadriceps) samples from three distinct (lanes 1–3) Chkb+/+ and three distinct (lanes 4–6) Chkb−/−mice probed with anti-vinculin, anti-itga7, anti-talin, anti-α-actinin, and anti-Gapdh antibodies. Bottom: densitometry of the Western blot data show the ratio of vinculin, metavinculin, itga7, talin, and a-actinin to Gapdh in forelimb (triceps) and hindlimb (quadriceps) samples. Values are means ± SD; n = 3–4 per group. *P < 0.05, **P < 0.01, ***P < 0.001 (t test). Detergent (NP40), soluble (cytosolic).

    Journal: Life science alliance

    Article Title: Defects in integrin complex formation promote CHKB -mediated muscular dystrophy.

    doi: 10.26508/lsa.202301956

    Figure Lengend Snippet: Figure 2. Decreased abundance and sarcolemma association of integrin-mediated linkage components in affected muscle of Chkb2/2 mice. (A, B) Western blot of total tissue lysis of (A) forelimb (triceps) and (B) hindlimb (quadriceps) samples from three distinct (lanes 1–3) Chkb+/+ and three distinct (lanes 4–6) Chkb−/−mice probed with anti-vinculin, anti-itga7, anti-talin, anti-α-actinin, and anti-Gapdh antibodies. Bottom: densitometry of the Western blot data show the ratio of vinculin, metavinculin, itga7, talin, and a-actinin to Gapdh in forelimb (triceps) and hindlimb (quadriceps) samples. Values are means ± SD; n = 3–4 per group. *P < 0.05, **P < 0.01, ***P < 0.001 (t test). Detergent (NP40), soluble (cytosolic).

    Article Snippet: GFP-mouse vinculin full length (889) was a gift from Alpha Yap (plasmid #67935; Addgene; http://n2t.net/addgene:67935; RRID:Addgene_67935), mRFP-Lact-C2 was a gift from Sergio Grinstein (plasmid #74061; Addgene; http://n2t.net/addgene:74061; RRID:Addgene_74061) and was previously described (52).

    Techniques: Western Blot, Lysis

    Figure 4. Treatment with choline kinase alpha inhibitors results in mis-localization of PI(4,5)P2 and decreases vinculin localization in focal adhesions in control U2OS cells but has no effect on U2OS cells overexpressing Myc-CHKB. (A) U2OS cells were transiently transfected with the PI(4,5)P2 reporter PH-PLCD1-GFP and were treated with the choline kinase alpha inhibitors EB-3D (10 mM), CK-37 (15 mM) or vehicle for 48 h and live cells were imaged by spinning-disk confocal microscopy. Choline kinase alpha inhibition resulted in the loss of dorsal membrane PH- PLCD1-GFP clusters in the U2OS cells. (B) The ratio of dorsal plasma membrane: cytoplasmic PH-PLCD1-GFP fluorescence is significantly decreased in choline kinase

    Journal: Life science alliance

    Article Title: Defects in integrin complex formation promote CHKB -mediated muscular dystrophy.

    doi: 10.26508/lsa.202301956

    Figure Lengend Snippet: Figure 4. Treatment with choline kinase alpha inhibitors results in mis-localization of PI(4,5)P2 and decreases vinculin localization in focal adhesions in control U2OS cells but has no effect on U2OS cells overexpressing Myc-CHKB. (A) U2OS cells were transiently transfected with the PI(4,5)P2 reporter PH-PLCD1-GFP and were treated with the choline kinase alpha inhibitors EB-3D (10 mM), CK-37 (15 mM) or vehicle for 48 h and live cells were imaged by spinning-disk confocal microscopy. Choline kinase alpha inhibition resulted in the loss of dorsal membrane PH- PLCD1-GFP clusters in the U2OS cells. (B) The ratio of dorsal plasma membrane: cytoplasmic PH-PLCD1-GFP fluorescence is significantly decreased in choline kinase

    Article Snippet: GFP-mouse vinculin full length (889) was a gift from Alpha Yap (plasmid #67935; Addgene; http://n2t.net/addgene:67935; RRID:Addgene_67935), mRFP-Lact-C2 was a gift from Sergio Grinstein (plasmid #74061; Addgene; http://n2t.net/addgene:74061; RRID:Addgene_74061) and was previously described (52).

    Techniques: Control, Transfection, Confocal Microscopy, Inhibition, Membrane, Clinical Proteomics

    (A) U2OS cells were transiently transfected with the PI(4,5)P 2 reporter PH-PLCD1-GFP and were treated with the choline kinase alpha inhibitors EB-3D (10 mM), CK-37 (15 mM) or vehicle for 48 h and live cells were imaged by spinning-disk confocal microscopy. Choline kinase alpha inhibition resulted in the loss of dorsal membrane PH-PLCD1-GFP clusters in the U2OS cells. (B) The ratio of dorsal plasma membrane: cytoplasmic PH-PLCD1-GFP fluorescence is significantly decreased in choline kinase inhibited cells than in vehicle-treated cells. (C) Quantification of PH-PLCD1-GFP fluorescence intensity at the plasma membrane in vehicle and choline kinase inhibited cells. Treatment with the choline kinase alpha inhibitors EB-3D and CK-37 resulted in reduced PH-PLCD1-GFP fluorescence intensity at the plasma membrane. Data show the mean ± SD (n = 10–18 cells per experiment, three independent experiments); (one-way ANOVA followed by Tukey’s Multiple Comparison Test; *** P < 0.001). (D) Choline kinase inhibition decreases focal adhesion number in U2OS cells. U2OS cells were transiently transfected with GFP-vinculin and were treated with choline kinase alpha inhibitors EB-3D (10 mM), CK-37(15 mM) or vehicle for 48 h and imaged by spinning-disk confocal microscopy. Scale bars: 10 μm. Treatment with choline kinase alpha inhibitors significantly reduced focal adhesion numbers in U2OS cells compared with vehicle-treated cells. (E) The ratio of focal adhesion:cytoplasmic GFP-vinculin fluorescence is significantly decreased in choline kinase inhibited cells than in vehicle-treated cells. Data show the mean ± SD (n = 10–18 cells per experiment, three independent experiments); (one-way ANOVA followed by Tukey’s Multiple Comparison Test; *** P < 0.001). (F) Overexpression of Myc- CHKB in U2OS cells by lentivirus-mediated gene expression system. 24 h after lentiviral transfection, Myc-CHKB protein expression was determined by Western blot analysis. GAPDH was used as an internal control. (G) Choline kinase alpha inhibition by EB-3D (10 mM) or CK-37(15 mM) for 48 h did not reduce the plasma membrane localization of PH-PLCD1-GFP clusters in U2OS cells overexpressing Myc-CHKB. (H) The ratio of dorsal plasma membrane: cytoplasmic PH-PLCD1-GFP fluorescence in vehicle and choline kinase alpha inhibited cells overexpressing Myc-CHKB. (I) PH-PLCD1-GFP fluorescence intensity at the plasma membrane in vehicle and choline kinase alpha inhibited cells overexpressing Myc-CHKB. Data show the mean ± SD (n = 10–18 cells per experiment, three independent experiments); (one-way ANOVA followed by Tukey’s Multiple Comparison Test; *** P < 0.001). (J) Choline kinase alpha inhibition by EB-3D (10 mM) or CK-37(15 mM) for 48 h was essentially without effect on focal adhesion numbers in U2OS cells transfected with Myc-CHKB. (K) The ratio of focal adhesion:cytoplasmic GFP-vinculin fluorescence is similar in vehicle or choline kinase inhibited cells. Data show the mean ± SD (n = 10 cells per experiment, three independent experiments); (one-way ANOVA followed by Tukey’s Multiple Comparison Test; ns, not significant). Scale bar = 15 μm. Two additional independent experiments produced the same results.

    Journal: Life Science Alliance

    Article Title: Defects in integrin complex formation promote CHKB -mediated muscular dystrophy

    doi: 10.26508/lsa.202301956

    Figure Lengend Snippet: (A) U2OS cells were transiently transfected with the PI(4,5)P 2 reporter PH-PLCD1-GFP and were treated with the choline kinase alpha inhibitors EB-3D (10 mM), CK-37 (15 mM) or vehicle for 48 h and live cells were imaged by spinning-disk confocal microscopy. Choline kinase alpha inhibition resulted in the loss of dorsal membrane PH-PLCD1-GFP clusters in the U2OS cells. (B) The ratio of dorsal plasma membrane: cytoplasmic PH-PLCD1-GFP fluorescence is significantly decreased in choline kinase inhibited cells than in vehicle-treated cells. (C) Quantification of PH-PLCD1-GFP fluorescence intensity at the plasma membrane in vehicle and choline kinase inhibited cells. Treatment with the choline kinase alpha inhibitors EB-3D and CK-37 resulted in reduced PH-PLCD1-GFP fluorescence intensity at the plasma membrane. Data show the mean ± SD (n = 10–18 cells per experiment, three independent experiments); (one-way ANOVA followed by Tukey’s Multiple Comparison Test; *** P < 0.001). (D) Choline kinase inhibition decreases focal adhesion number in U2OS cells. U2OS cells were transiently transfected with GFP-vinculin and were treated with choline kinase alpha inhibitors EB-3D (10 mM), CK-37(15 mM) or vehicle for 48 h and imaged by spinning-disk confocal microscopy. Scale bars: 10 μm. Treatment with choline kinase alpha inhibitors significantly reduced focal adhesion numbers in U2OS cells compared with vehicle-treated cells. (E) The ratio of focal adhesion:cytoplasmic GFP-vinculin fluorescence is significantly decreased in choline kinase inhibited cells than in vehicle-treated cells. Data show the mean ± SD (n = 10–18 cells per experiment, three independent experiments); (one-way ANOVA followed by Tukey’s Multiple Comparison Test; *** P < 0.001). (F) Overexpression of Myc- CHKB in U2OS cells by lentivirus-mediated gene expression system. 24 h after lentiviral transfection, Myc-CHKB protein expression was determined by Western blot analysis. GAPDH was used as an internal control. (G) Choline kinase alpha inhibition by EB-3D (10 mM) or CK-37(15 mM) for 48 h did not reduce the plasma membrane localization of PH-PLCD1-GFP clusters in U2OS cells overexpressing Myc-CHKB. (H) The ratio of dorsal plasma membrane: cytoplasmic PH-PLCD1-GFP fluorescence in vehicle and choline kinase alpha inhibited cells overexpressing Myc-CHKB. (I) PH-PLCD1-GFP fluorescence intensity at the plasma membrane in vehicle and choline kinase alpha inhibited cells overexpressing Myc-CHKB. Data show the mean ± SD (n = 10–18 cells per experiment, three independent experiments); (one-way ANOVA followed by Tukey’s Multiple Comparison Test; *** P < 0.001). (J) Choline kinase alpha inhibition by EB-3D (10 mM) or CK-37(15 mM) for 48 h was essentially without effect on focal adhesion numbers in U2OS cells transfected with Myc-CHKB. (K) The ratio of focal adhesion:cytoplasmic GFP-vinculin fluorescence is similar in vehicle or choline kinase inhibited cells. Data show the mean ± SD (n = 10 cells per experiment, three independent experiments); (one-way ANOVA followed by Tukey’s Multiple Comparison Test; ns, not significant). Scale bar = 15 μm. Two additional independent experiments produced the same results.

    Article Snippet: GFP-mouse vinculin full length (889) was a gift from Alpha Yap (plasmid #67935; Addgene; http://n2t.net/addgene:67935 ; RRID:Addgene_67935), mRFP-Lact-C2 was a gift from Sergio Grinstein (plasmid #74061; Addgene; http://n2t.net/addgene:74061 ; RRID:Addgene_74061) and was previously described ( ).

    Techniques: Transfection, Confocal Microscopy, Inhibition, Membrane, Clinical Proteomics, Fluorescence, Comparison, Over Expression, Gene Expression, Expressing, Western Blot, Control, Produced

    (A, B) U2OS cells were transiently co-transfected with the PI(4,5)P 2 reporter PH-PLCD1-GFP and PS reporter mRFP-Lact-C2 and were treated with DMSO (vehicle control) or the choline kinase alpha inhibitor EB-3D (15 mM) for 48 h and imaged by spinning-disk confocal microscopy in live cells. Choline kinase inhibition resulted in internalization of dorsal plasma membrane PH-PLCD1-GFP fluorescence where it colocalized PS containing organelles. Scale bar = 15 μm. (C) Quantification of the ratio of dorsal plasma membrane: cytoplasmic PS reporter mRFP-Lact-C2. (D, E) Quantification of the fraction of PI(4,5)P 2 overlapping PS (D),and the fraction of PS overlapping PI(4,5)P 2 (E) using the Manders’ colocalization coefficients in vehicle-treated and choline kinase inhibited cells. (F) Colocalization between PI(4,5)P 2 and PS quantified as Pearson's correlation coefficient in vehicle-treated and choline kinase inhibited cells. For (C, D, E, F) data show the mean ± SD. N = 25 random cells per group. * P < 0.05, ** P < 0.01, *** P < 0.001 ( t test).

    Journal: Life Science Alliance

    Article Title: Defects in integrin complex formation promote CHKB -mediated muscular dystrophy

    doi: 10.26508/lsa.202301956

    Figure Lengend Snippet: (A, B) U2OS cells were transiently co-transfected with the PI(4,5)P 2 reporter PH-PLCD1-GFP and PS reporter mRFP-Lact-C2 and were treated with DMSO (vehicle control) or the choline kinase alpha inhibitor EB-3D (15 mM) for 48 h and imaged by spinning-disk confocal microscopy in live cells. Choline kinase inhibition resulted in internalization of dorsal plasma membrane PH-PLCD1-GFP fluorescence where it colocalized PS containing organelles. Scale bar = 15 μm. (C) Quantification of the ratio of dorsal plasma membrane: cytoplasmic PS reporter mRFP-Lact-C2. (D, E) Quantification of the fraction of PI(4,5)P 2 overlapping PS (D),and the fraction of PS overlapping PI(4,5)P 2 (E) using the Manders’ colocalization coefficients in vehicle-treated and choline kinase inhibited cells. (F) Colocalization between PI(4,5)P 2 and PS quantified as Pearson's correlation coefficient in vehicle-treated and choline kinase inhibited cells. For (C, D, E, F) data show the mean ± SD. N = 25 random cells per group. * P < 0.05, ** P < 0.01, *** P < 0.001 ( t test).

    Article Snippet: GFP-mouse vinculin full length (889) was a gift from Alpha Yap (plasmid #67935; Addgene; http://n2t.net/addgene:67935 ; RRID:Addgene_67935), mRFP-Lact-C2 was a gift from Sergio Grinstein (plasmid #74061; Addgene; http://n2t.net/addgene:74061 ; RRID:Addgene_74061) and was previously described ( ).

    Techniques: Transfection, Control, Confocal Microscopy, Inhibition, Clinical Proteomics, Membrane, Fluorescence

    Live-cell images of two cells expressing both (a, d) green fluorescent vinculin and (b, e) red fluorescent actin seeded upon (a-c) fibronectin coated glass and (d-f) transparent 6.5±0.4 μm long TiO 2 NT platforms, with (c, f) vinculin and actin images overlaid. Acquisition and display settings were identical between (a-c) and (d-f).

    Journal: bioRxiv

    Article Title: Transparent Titanium Dioxide Nanotubes: Processing, Characterization, and Application in Establishing Cellular Response Mechanisms

    doi: 10.1101/330712

    Figure Lengend Snippet: Live-cell images of two cells expressing both (a, d) green fluorescent vinculin and (b, e) red fluorescent actin seeded upon (a-c) fibronectin coated glass and (d-f) transparent 6.5±0.4 μm long TiO 2 NT platforms, with (c, f) vinculin and actin images overlaid. Acquisition and display settings were identical between (a-c) and (d-f).

    Article Snippet: DH5alpha strain of E. coli with GFP-mouse vinculin (Cat. #67935) and mCherry-UtrCH (Cat. #26740) bacterial stabs (plasmids) were purchased from Addgene, Cambridge, MA.

    Techniques: Expressing