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alexa647 human transferrin  (Thermo Fisher)


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    Thermo Fisher alexa647 human transferrin
    Alexa647 Human Transferrin, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/alexa647+human+transferrin/Transferrin/bio_rxiv__64898__2026__03__17__712024-252-25-27
    Average 99 stars, based on 1 article reviews
    alexa647 human transferrin - by Bioz Stars, 2026-09
    99/100 stars

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    Labeling:

    Article Title: Dynein-dependent positioning of multiple organelles regulates adaptive gene expression during oxidative stress
    Article Snippet: .. For labeling of lysosomes, mitochondria or recycling endosomes, cells were treated, respectively, with LysoTrackerTM (Thermo Fisher Scientific) MitoTrackerTM Deep Red FM (Thermo Fisher Scientific) or Alexa647-human transferrin (Thermo Fisher Scientific; 30 min pretreatment to allow trafficking of transferrin to the recycling endosome compartment). ..



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    A) PV1 does not colocalize with clathrin-GFP on the cell surface. Confocal micrographs of MLEC-WT transfected with clathrin-GFP ( Clathrin, green ) and labeled with fluorescent anti-PV1 antibodies ( PV1, red ). The insets represent a low power field with two transfected cells. The areas in shaded in grey are magnified in lowed panels. B–G) PV1 and transferrin internalization rates in MLECs were quantified by flow cytometry. Error bars correspond to StDev. B–D) Percentage of fluorescent antibody labeled PV1 internalized from the cell surface. B) PV1 internalization at 15 and 60 min in presence and absence of the clathrin pathway inhibitor PitStop2 ( PS2 ) or the inactive PitStop2 negative control ( NC ) (n = 4, p >0.05). C,D) PV1 internalization at 15 and 60 min in presence of dynamin inhibitors Dyngo-4a (C) (n = 4, p >0.05) or Dynasore ( D ) (n = 4, p>0.05). E) Median fluorescent intensity of <t>transferrin-Alexa647</t> internalized within 10 min in the presence and absence of PitStop2, Dynasore or Dyngo4a (n = 4, * p <0.01). D–G) Internalization of PV1 (F) and transferrin (G) at 15 min in untransfected MLECs (mock) and MLECs transfected with eGFP-encoding plasmid (GFP), dynamin 2-eGFP fusion (Dyn2 wt) or dominant-negative form of dynamin 2 fused to eGFP (Dyn2 K44A MLECs (n = 4, * p <0.01). H) Schematic of PV1 ( green ) trafficking in ECs. De novo formed PV1 enters the secretory pathway and arrives at the cell surface by exocytosis ( green arrow ) using secretory vesicles (Step 1). On the plasma membrane PV1 is targeted to caveolae, fenestrae or TEC (Step 2) where it forms diaphragms. PV1 is internalized via clathrin- and dynamin-independent endocytic mechanism ( Step 3 and 4 ) followed by degradation in the lysosomes ( Step 5 ).
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    A) PV1 does not colocalize with clathrin-GFP on the cell surface. Confocal micrographs of MLEC-WT transfected with clathrin-GFP ( Clathrin, green ) and labeled with fluorescent anti-PV1 antibodies ( PV1, red ). The insets represent a low power field with two transfected cells. The areas in shaded in grey are magnified in lowed panels. B–G) PV1 and transferrin internalization rates in MLECs were quantified by flow cytometry. Error bars correspond to StDev. B–D) Percentage of fluorescent antibody labeled PV1 internalized from the cell surface. B) PV1 internalization at 15 and 60 min in presence and absence of the clathrin pathway inhibitor PitStop2 ( PS2 ) or the inactive PitStop2 negative control ( NC ) (n = 4, p >0.05). C,D) PV1 internalization at 15 and 60 min in presence of dynamin inhibitors Dyngo-4a (C) (n = 4, p >0.05) or Dynasore ( D ) (n = 4, p>0.05). E) Median fluorescent intensity of <t>transferrin-Alexa647</t> internalized within 10 min in the presence and absence of PitStop2, Dynasore or Dyngo4a (n = 4, * p <0.01). D–G) Internalization of PV1 (F) and transferrin (G) at 15 min in untransfected MLECs (mock) and MLECs transfected with eGFP-encoding plasmid (GFP), dynamin 2-eGFP fusion (Dyn2 wt) or dominant-negative form of dynamin 2 fused to eGFP (Dyn2 K44A MLECs (n = 4, * p <0.01). H) Schematic of PV1 ( green ) trafficking in ECs. De novo formed PV1 enters the secretory pathway and arrives at the cell surface by exocytosis ( green arrow ) using secretory vesicles (Step 1). On the plasma membrane PV1 is targeted to caveolae, fenestrae or TEC (Step 2) where it forms diaphragms. PV1 is internalized via clathrin- and dynamin-independent endocytic mechanism ( Step 3 and 4 ) followed by degradation in the lysosomes ( Step 5 ).
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    A) PV1 does not colocalize with clathrin-GFP on the cell surface. Confocal micrographs of MLEC-WT transfected with clathrin-GFP ( Clathrin, green ) and labeled with fluorescent anti-PV1 antibodies ( PV1, red ). The insets represent a low power field with two transfected cells. The areas in shaded in grey are magnified in lowed panels. B–G) PV1 and transferrin internalization rates in MLECs were quantified by flow cytometry. Error bars correspond to StDev. B–D) Percentage of fluorescent antibody labeled PV1 internalized from the cell surface. B) PV1 internalization at 15 and 60 min in presence and absence of the clathrin pathway inhibitor PitStop2 ( PS2 ) or the inactive PitStop2 negative control ( NC ) (n = 4, p >0.05). C,D) PV1 internalization at 15 and 60 min in presence of dynamin inhibitors Dyngo-4a (C) (n = 4, p >0.05) or Dynasore ( D ) (n = 4, p>0.05). E) Median fluorescent intensity of <t>transferrin-Alexa647</t> internalized within 10 min in the presence and absence of PitStop2, Dynasore or Dyngo4a (n = 4, * p <0.01). D–G) Internalization of PV1 (F) and transferrin (G) at 15 min in untransfected MLECs (mock) and MLECs transfected with eGFP-encoding plasmid (GFP), dynamin 2-eGFP fusion (Dyn2 wt) or dominant-negative form of dynamin 2 fused to eGFP (Dyn2 K44A MLECs (n = 4, * p <0.01). H) Schematic of PV1 ( green ) trafficking in ECs. De novo formed PV1 enters the secretory pathway and arrives at the cell surface by exocytosis ( green arrow ) using secretory vesicles (Step 1). On the plasma membrane PV1 is targeted to caveolae, fenestrae or TEC (Step 2) where it forms diaphragms. PV1 is internalized via clathrin- and dynamin-independent endocytic mechanism ( Step 3 and 4 ) followed by degradation in the lysosomes ( Step 5 ).
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    Image Search Results


    A) PV1 does not colocalize with clathrin-GFP on the cell surface. Confocal micrographs of MLEC-WT transfected with clathrin-GFP ( Clathrin, green ) and labeled with fluorescent anti-PV1 antibodies ( PV1, red ). The insets represent a low power field with two transfected cells. The areas in shaded in grey are magnified in lowed panels. B–G) PV1 and transferrin internalization rates in MLECs were quantified by flow cytometry. Error bars correspond to StDev. B–D) Percentage of fluorescent antibody labeled PV1 internalized from the cell surface. B) PV1 internalization at 15 and 60 min in presence and absence of the clathrin pathway inhibitor PitStop2 ( PS2 ) or the inactive PitStop2 negative control ( NC ) (n = 4, p >0.05). C,D) PV1 internalization at 15 and 60 min in presence of dynamin inhibitors Dyngo-4a (C) (n = 4, p >0.05) or Dynasore ( D ) (n = 4, p>0.05). E) Median fluorescent intensity of transferrin-Alexa647 internalized within 10 min in the presence and absence of PitStop2, Dynasore or Dyngo4a (n = 4, * p <0.01). D–G) Internalization of PV1 (F) and transferrin (G) at 15 min in untransfected MLECs (mock) and MLECs transfected with eGFP-encoding plasmid (GFP), dynamin 2-eGFP fusion (Dyn2 wt) or dominant-negative form of dynamin 2 fused to eGFP (Dyn2 K44A MLECs (n = 4, * p <0.01). H) Schematic of PV1 ( green ) trafficking in ECs. De novo formed PV1 enters the secretory pathway and arrives at the cell surface by exocytosis ( green arrow ) using secretory vesicles (Step 1). On the plasma membrane PV1 is targeted to caveolae, fenestrae or TEC (Step 2) where it forms diaphragms. PV1 is internalized via clathrin- and dynamin-independent endocytic mechanism ( Step 3 and 4 ) followed by degradation in the lysosomes ( Step 5 ).

    Journal: PLoS ONE

    Article Title: Caveolae, Fenestrae and Transendothelial Channels Retain PV1 on the Surface of Endothelial Cells

    doi: 10.1371/journal.pone.0032655

    Figure Lengend Snippet: A) PV1 does not colocalize with clathrin-GFP on the cell surface. Confocal micrographs of MLEC-WT transfected with clathrin-GFP ( Clathrin, green ) and labeled with fluorescent anti-PV1 antibodies ( PV1, red ). The insets represent a low power field with two transfected cells. The areas in shaded in grey are magnified in lowed panels. B–G) PV1 and transferrin internalization rates in MLECs were quantified by flow cytometry. Error bars correspond to StDev. B–D) Percentage of fluorescent antibody labeled PV1 internalized from the cell surface. B) PV1 internalization at 15 and 60 min in presence and absence of the clathrin pathway inhibitor PitStop2 ( PS2 ) or the inactive PitStop2 negative control ( NC ) (n = 4, p >0.05). C,D) PV1 internalization at 15 and 60 min in presence of dynamin inhibitors Dyngo-4a (C) (n = 4, p >0.05) or Dynasore ( D ) (n = 4, p>0.05). E) Median fluorescent intensity of transferrin-Alexa647 internalized within 10 min in the presence and absence of PitStop2, Dynasore or Dyngo4a (n = 4, * p <0.01). D–G) Internalization of PV1 (F) and transferrin (G) at 15 min in untransfected MLECs (mock) and MLECs transfected with eGFP-encoding plasmid (GFP), dynamin 2-eGFP fusion (Dyn2 wt) or dominant-negative form of dynamin 2 fused to eGFP (Dyn2 K44A MLECs (n = 4, * p <0.01). H) Schematic of PV1 ( green ) trafficking in ECs. De novo formed PV1 enters the secretory pathway and arrives at the cell surface by exocytosis ( green arrow ) using secretory vesicles (Step 1). On the plasma membrane PV1 is targeted to caveolae, fenestrae or TEC (Step 2) where it forms diaphragms. PV1 is internalized via clathrin- and dynamin-independent endocytic mechanism ( Step 3 and 4 ) followed by degradation in the lysosomes ( Step 5 ).

    Article Snippet: Positive controls for each inhibitor effectiveness consisted of Alexa647 labeled human transferrin or EGF (Invitrogen, Molecular Probes).

    Techniques: Transfection, Labeling, Flow Cytometry, Negative Control, Plasmid Preparation, Dominant Negative Mutation