polyclonal rabbit anti cx43  (Thermo Fisher)


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  • 95
    Name:
    Connexin 43 Polyclonal Antibody
    Description:
    Connexin 43 Polyclonal Antibody for Western Blot IF IHC P ELISA
    Catalog Number:
    710700
    Price:
    None
    Applications:
    Build Your Own Immunoassay|Cell Analysis|Cell Junctions|Cellular Imaging|ELISA|Gap Junctions|IHC Staining & Detection|Immunocytochemistry (ICC)|Immunofluorescence (IF)|Immunofluorescence Staining & Detection|Immunohistochemistry (IHC)|Protein Assays and Analysis|Protein Biology|Western Blot Detection|Western Blotting|Cell Structure
    Category:
    Antibodies Secondary Detection Reagents
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    Structured Review

    Thermo Fisher polyclonal rabbit anti cx43
    Connexin 43 Polyclonal Antibody for Western Blot IF IHC P ELISA
    https://www.bioz.com/result/polyclonal rabbit anti cx43/product/Thermo Fisher
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    polyclonal rabbit anti cx43 - by Bioz Stars, 2020-08
    95/100 stars

    Images

    Related Articles

    Incubation:

    Article Title: Tamoxifen and raloxifene modulate gap junction coupling during early phases of retinoic acid-dependent neuronal differentiation of NTera2/D1 cells
    Article Snippet: .. After washing and permeabilization with PBS/Tween-20 they were blocked with 0.5% goat serum in PBS/Tween-20, and incubated over night at 4°C with primary antibodies directed to either Cx43 (rabbit polyclonal, 1:400; http://www.invitrogen.com ) or βIII-tubulin (rabbit polyclonal, 1:100; http://www.sigmaaldrich.com ). .. For visualization, fixed cells were incubated sequentially with a biotinylated goat anti-rabbit secondary antibody (dilution 1:400; http://www.sigmaaldrich.com ), followed by a complex of fluorescein-isothiocyanate and streptavidin (dilution 1:400; http://www.sigmaaldrich.com ).

    Article Title: Olfactory ensheathing cell membrane properties are shaped by connectivity
    Article Snippet: .. Primary antibodies [rabbit anti-BLBP, AB9558; rat anti-NCAM, MAB310; mouse anti-connexin 32 (Cx32), MAB3069; and rabbit anti-Cx26, AB1717 from Chemicon/Millipore; rabbit anti-Cx43 71-0700 from Zymed/Invitrogen] diluted in blocking buffer were incubated overnight at room temperature. .. Sections were washed 3 times in 0.3% Triton X-100 in PBS for 10 minutes and incubated in secondary antibodies conjugated to Alexa Fluor (Invitrogen/Molecular Probes, Carlsbad, CA) and DRAQ5, diluted 1:1000 in blocking buffer for 2 hours at room temperature.

    Article Title: Loss of connexin43 in murine Sertoli cells and its effect on blood-testis barrier formation and dynamics
    Article Snippet: .. Both primary antibodies were diluted in 1% BSA in PBS and incubated overnight at 4°C in a humidified chamber: beta-galactosidase (Abcam ab616, 1:3000), Cx43 (Invitrogen 71–0700, 1:250). .. On the following day, sections were incubated for 45 min with horseradish peroxidase (HRP)-conjugated secondary antibody (anti-rabbit EnVision; DAKO, Hamburg, Germany, ready to use) and immunoreaction was visualised by diaminobenzidin (DAB; EnVision, Dako, Hamburg, Germany).

    Article Title: Mitochondrial connexin40 regulates mitochondrial calcium uptake in coronary endothelial cells
    Article Snippet: .. Blots were incubated with the following primary antibodies: anti-Cx40 (Santa Cruz, sc-20466; 1:2,000), anti-ATP5A (Santa Cruz, sc-136178; 1:2,000), anti-Actin (Santa Cruz, sc-1616; 1:4,000), anti-Cx37 (Thermo Fisher Scientific, 42-4400; 1:1,000), anti-Cx43 (Thermo Fisher Scientific, 71-0700; 1:2,000), anti-Cx45 (Thermo Fisher Scientific, 41-5800; 1:2,000), or anti-GAPDH (Thermo Fisher Scientific, MA5-15738; 1:4,000), followed by horseradish peroxidase-linked secondary antibody incubation. .. The immunoblots were identified with the SuperSignal West Pico Chemiluminescent Substrate (Thermo Fisher Scientific, 34087).

    Article Title: Reciprocal Regulation of Epileptiform Neuronal Oscillations and Electrical Synapses in the Rat Hippocampus
    Article Snippet: .. After rinsed in TBST, blots were incubated overnight with primary antibodies raised against Cx36 (rabbit polyclonal 36-4600, Zymed/Invitrogen, 1∶1000), Cx45 (rabbit polyclonal AB1745, Millipore, Billerica, MA, USA, 1∶1000), Cx43 (rabbit polyclonal 71-0700, mouse monoclonal 13-8300, Zymed/Invitrogen, 1∶1000) and beta-actin (mouse monoclonal A5316, Sigma-Aldrich, 1∶10000) diluted in TBST/3% non-fat milk. .. After the primary antibody incubation, blots were rinsed in TBST and incubated with the appropriate secondary antibody raised against rabbit or mouse conjugated to horseradish peroxidase (HRP) enzyme (1∶5000, Invitrogen, Carlsbad, CA, USA) for 2 h at room temperature.

    SDS Page:

    Article Title: Tanshinone IIA Increases the Bystander Effect of Herpes Simplex Virus Thymidine Kinase/Ganciclovir Gene Therapy via Enhanced Gap Junctional Intercellular Communication
    Article Snippet: .. Total cell extracts were subjected to 10% SDS-PAGE, and immunoblotted using anti-Cx26 (CX-12H10; Zymed, San Francisco, CA, USA ), anti-Cx30 (71-2200; Zymed, San Francisco, CA, USA) anti-Cx43 (71-0700; Zymed, San Francisco, CA, USA) or anti-actin (ms-1295-po, NeoMarkers, CA, USA). .. Functional Assay of GJIC GJIC function of was examined by the fluorescent dye transfer method as described by Goldberg with minor modification .

    Mass Spectrometry:

    Article Title: Tanshinone IIA Increases the Bystander Effect of Herpes Simplex Virus Thymidine Kinase/Ganciclovir Gene Therapy via Enhanced Gap Junctional Intercellular Communication
    Article Snippet: .. Total cell extracts were subjected to 10% SDS-PAGE, and immunoblotted using anti-Cx26 (CX-12H10; Zymed, San Francisco, CA, USA ), anti-Cx30 (71-2200; Zymed, San Francisco, CA, USA) anti-Cx43 (71-0700; Zymed, San Francisco, CA, USA) or anti-actin (ms-1295-po, NeoMarkers, CA, USA). .. Functional Assay of GJIC GJIC function of was examined by the fluorescent dye transfer method as described by Goldberg with minor modification .

    Blocking Assay:

    Article Title: Olfactory ensheathing cell membrane properties are shaped by connectivity
    Article Snippet: .. Primary antibodies [rabbit anti-BLBP, AB9558; rat anti-NCAM, MAB310; mouse anti-connexin 32 (Cx32), MAB3069; and rabbit anti-Cx26, AB1717 from Chemicon/Millipore; rabbit anti-Cx43 71-0700 from Zymed/Invitrogen] diluted in blocking buffer were incubated overnight at room temperature. .. Sections were washed 3 times in 0.3% Triton X-100 in PBS for 10 minutes and incubated in secondary antibodies conjugated to Alexa Fluor (Invitrogen/Molecular Probes, Carlsbad, CA) and DRAQ5, diluted 1:1000 in blocking buffer for 2 hours at room temperature.

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  • 92
    Thermo Fisher rabbit anti phospho cx43 ser373
    Schematic showing potential roles of astrocytic <t>Cx43,</t> hemichannels, and GJIC during OGD/R injury. Under normal conditions, astrocytic Cx43 is expressed in the plasma membrane and assembled into hemichannels that are normally closed. Hemichannel-hemichannel interactions induce the formation of GJIC between adjacent astrocytes, which permits the exchange of ions and small molecules; also, plasma membrane’s Cx43 was phosphorylated at Ser368 site. In such circumstances, astrocytes, together with those resting microglia, function as a supportive assistant for healthy neurons. OGD/R injury caused abnormal hemichannel opening and consequent substantial astrocytic ATP release. It also induced microglial activation with a predominance of the pro-inflammatory cytokine-releasing M1 subtype. Extracellular ATP induced further microglial activation and pro-inflammatory cytokine release, and these pro-inflammatory cytokines induced further opening of astrocytic hemichannels. SalB reversed these effects and thus provided protection against OGD/R injury. This suggests the existence of a vicious cycle in which astrocytic hemichannel opening and pro-inflammatory microglial activation reinforce each other following OGD/R injury. This vicious cycle may account for secondary injury and extended damage after OGD/R injury; OGD/R injury caused gap junction internalization, which may account for the astrocytic uncoupling events. It also decreased plasma membrane levels of Ser368-phosphorylated Cx43 while increasing plasma membrane levels of <t>Ser373-phosphorylated</t> Cx43, Ser265-phosphorylated Cx43, and Src’s Tyr416-phosphorylated activated form. The activated Src may well have phosphorylated Cx43 at Tyr265 and further induced gap junction internalization or autophagy. SalB directly inhibits Src, which may allow it to exert protective effects by attenuating Cx43 internalization. CBX, a non-selective hemichannel and GJIC inhibitor, did not apparently affect Cx43 phosphorylation, but it inhibited PKC and Src activity
    Rabbit Anti Phospho Cx43 Ser373, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti phospho cx43 ser373/product/Thermo Fisher
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti phospho cx43 ser373 - by Bioz Stars, 2020-08
    92/100 stars
      Buy from Supplier

    94
    Thermo Fisher rabbit polyclonal anti connexin43 antibody
    Schematic showing potential roles of astrocytic <t>Cx43,</t> hemichannels, and GJIC during OGD/R injury. Under normal conditions, astrocytic Cx43 is expressed in the plasma membrane and assembled into hemichannels that are normally closed. Hemichannel-hemichannel interactions induce the formation of GJIC between adjacent astrocytes, which permits the exchange of ions and small molecules; also, plasma membrane’s Cx43 was phosphorylated at Ser368 site. In such circumstances, astrocytes, together with those resting microglia, function as a supportive assistant for healthy neurons. OGD/R injury caused abnormal hemichannel opening and consequent substantial astrocytic ATP release. It also induced microglial activation with a predominance of the pro-inflammatory cytokine-releasing M1 subtype. Extracellular ATP induced further microglial activation and pro-inflammatory cytokine release, and these pro-inflammatory cytokines induced further opening of astrocytic hemichannels. SalB reversed these effects and thus provided protection against OGD/R injury. This suggests the existence of a vicious cycle in which astrocytic hemichannel opening and pro-inflammatory microglial activation reinforce each other following OGD/R injury. This vicious cycle may account for secondary injury and extended damage after OGD/R injury; OGD/R injury caused gap junction internalization, which may account for the astrocytic uncoupling events. It also decreased plasma membrane levels of Ser368-phosphorylated Cx43 while increasing plasma membrane levels of <t>Ser373-phosphorylated</t> Cx43, Ser265-phosphorylated Cx43, and Src’s Tyr416-phosphorylated activated form. The activated Src may well have phosphorylated Cx43 at Tyr265 and further induced gap junction internalization or autophagy. SalB directly inhibits Src, which may allow it to exert protective effects by attenuating Cx43 internalization. CBX, a non-selective hemichannel and GJIC inhibitor, did not apparently affect Cx43 phosphorylation, but it inhibited PKC and Src activity
    Rabbit Polyclonal Anti Connexin43 Antibody, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit polyclonal anti connexin43 antibody/product/Thermo Fisher
    Average 94 stars, based on 2 article reviews
    Price from $9.99 to $1999.99
    rabbit polyclonal anti connexin43 antibody - by Bioz Stars, 2020-08
    94/100 stars
      Buy from Supplier

    92
    Thermo Fisher rabbit anti phospho cx43
    Schematic showing potential roles of astrocytic <t>Cx43,</t> hemichannels, and GJIC during OGD/R injury. Under normal conditions, astrocytic Cx43 is expressed in the plasma membrane and assembled into hemichannels that are normally closed. Hemichannel-hemichannel interactions induce the formation of GJIC between adjacent astrocytes, which permits the exchange of ions and small molecules; also, plasma membrane’s Cx43 was phosphorylated at Ser368 site. In such circumstances, astrocytes, together with those resting microglia, function as a supportive assistant for healthy neurons. OGD/R injury caused abnormal hemichannel opening and consequent substantial astrocytic ATP release. It also induced microglial activation with a predominance of the pro-inflammatory cytokine-releasing M1 subtype. Extracellular ATP induced further microglial activation and pro-inflammatory cytokine release, and these pro-inflammatory cytokines induced further opening of astrocytic hemichannels. SalB reversed these effects and thus provided protection against OGD/R injury. This suggests the existence of a vicious cycle in which astrocytic hemichannel opening and pro-inflammatory microglial activation reinforce each other following OGD/R injury. This vicious cycle may account for secondary injury and extended damage after OGD/R injury; OGD/R injury caused gap junction internalization, which may account for the astrocytic uncoupling events. It also decreased plasma membrane levels of Ser368-phosphorylated Cx43 while increasing plasma membrane levels of <t>Ser373-phosphorylated</t> Cx43, Ser265-phosphorylated Cx43, and Src’s Tyr416-phosphorylated activated form. The activated Src may well have phosphorylated Cx43 at Tyr265 and further induced gap junction internalization or autophagy. SalB directly inhibits Src, which may allow it to exert protective effects by attenuating Cx43 internalization. CBX, a non-selective hemichannel and GJIC inhibitor, did not apparently affect Cx43 phosphorylation, but it inhibited PKC and Src activity
    Rabbit Anti Phospho Cx43, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti phospho cx43/product/Thermo Fisher
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti phospho cx43 - by Bioz Stars, 2020-08
    92/100 stars
      Buy from Supplier

    Image Search Results


    Schematic showing potential roles of astrocytic Cx43, hemichannels, and GJIC during OGD/R injury. Under normal conditions, astrocytic Cx43 is expressed in the plasma membrane and assembled into hemichannels that are normally closed. Hemichannel-hemichannel interactions induce the formation of GJIC between adjacent astrocytes, which permits the exchange of ions and small molecules; also, plasma membrane’s Cx43 was phosphorylated at Ser368 site. In such circumstances, astrocytes, together with those resting microglia, function as a supportive assistant for healthy neurons. OGD/R injury caused abnormal hemichannel opening and consequent substantial astrocytic ATP release. It also induced microglial activation with a predominance of the pro-inflammatory cytokine-releasing M1 subtype. Extracellular ATP induced further microglial activation and pro-inflammatory cytokine release, and these pro-inflammatory cytokines induced further opening of astrocytic hemichannels. SalB reversed these effects and thus provided protection against OGD/R injury. This suggests the existence of a vicious cycle in which astrocytic hemichannel opening and pro-inflammatory microglial activation reinforce each other following OGD/R injury. This vicious cycle may account for secondary injury and extended damage after OGD/R injury; OGD/R injury caused gap junction internalization, which may account for the astrocytic uncoupling events. It also decreased plasma membrane levels of Ser368-phosphorylated Cx43 while increasing plasma membrane levels of Ser373-phosphorylated Cx43, Ser265-phosphorylated Cx43, and Src’s Tyr416-phosphorylated activated form. The activated Src may well have phosphorylated Cx43 at Tyr265 and further induced gap junction internalization or autophagy. SalB directly inhibits Src, which may allow it to exert protective effects by attenuating Cx43 internalization. CBX, a non-selective hemichannel and GJIC inhibitor, did not apparently affect Cx43 phosphorylation, but it inhibited PKC and Src activity

    Journal: Journal of Neuroinflammation

    Article Title: Roles of astrocytic connexin-43, hemichannels, and gap junctions in oxygen-glucose deprivation/reperfusion injury induced neuroinflammation and the possible regulatory mechanisms of salvianolic acid B and carbenoxolone

    doi: 10.1186/s12974-018-1127-3

    Figure Lengend Snippet: Schematic showing potential roles of astrocytic Cx43, hemichannels, and GJIC during OGD/R injury. Under normal conditions, astrocytic Cx43 is expressed in the plasma membrane and assembled into hemichannels that are normally closed. Hemichannel-hemichannel interactions induce the formation of GJIC between adjacent astrocytes, which permits the exchange of ions and small molecules; also, plasma membrane’s Cx43 was phosphorylated at Ser368 site. In such circumstances, astrocytes, together with those resting microglia, function as a supportive assistant for healthy neurons. OGD/R injury caused abnormal hemichannel opening and consequent substantial astrocytic ATP release. It also induced microglial activation with a predominance of the pro-inflammatory cytokine-releasing M1 subtype. Extracellular ATP induced further microglial activation and pro-inflammatory cytokine release, and these pro-inflammatory cytokines induced further opening of astrocytic hemichannels. SalB reversed these effects and thus provided protection against OGD/R injury. This suggests the existence of a vicious cycle in which astrocytic hemichannel opening and pro-inflammatory microglial activation reinforce each other following OGD/R injury. This vicious cycle may account for secondary injury and extended damage after OGD/R injury; OGD/R injury caused gap junction internalization, which may account for the astrocytic uncoupling events. It also decreased plasma membrane levels of Ser368-phosphorylated Cx43 while increasing plasma membrane levels of Ser373-phosphorylated Cx43, Ser265-phosphorylated Cx43, and Src’s Tyr416-phosphorylated activated form. The activated Src may well have phosphorylated Cx43 at Tyr265 and further induced gap junction internalization or autophagy. SalB directly inhibits Src, which may allow it to exert protective effects by attenuating Cx43 internalization. CBX, a non-selective hemichannel and GJIC inhibitor, did not apparently affect Cx43 phosphorylation, but it inhibited PKC and Src activity

    Article Snippet: Western blot analysis Protein concentration was evaluated using the BCA method, and 20–40 μg of total extract was separated on SDS polyacrilamide gels, and then the gel-separated proteins were transferred onto polyvinylidene fluoride (PVDF) membranes and probed using the indicated primary antibodies: overnight at 4 °C with Rabbit anti-pan Cx43(1:1000, Cell signaling technology, Cat#3512); Rabbit anti-phospho-Cx43/ GJA1(Ser 368)(1:1000, Abcam,Cat#ab30559); Rabbit anti-phospho-Cx43 (Ser373) (1:1000, Thermo Fisher Scientific, Cat#PA5-64670); Rabbit anti-phospho-Cx43(Ser265)(1:500, Thermo Fisher Scientific, Cat#PA5-37584); Rabbit anti-PKCε (1:200, Santa Cruz Biotechnology, Cat#sc-214); Goat anti-phospho-PKCε (Ser729) (1: 200, Santa Cruz Biotechnology, Cat#sc-12355); Rabbit anti-Akt(PKB) (1:1000, Cell Signaling Technology, Cat#4691); Rabbit anti-phospho-Akt(Thr308) antibody (1:1000, Cell Signaling Technology, Cat#13038); Rabbit anti-Src (1:1000, Cell Signaling Technology, Cat#2108); Rabbit anti-Phospho-Src(Tyr527) (1:1000, Cell Signaling Technology, Cat#2105); Rabbit anti-Phospho-Src(Tyr416) (1:1000, Cell Signaling Technology, Cat#6943); Rabbit anti-GAPDH antibody (1/5000, Abcam, Cat#ab37168); mouse anti-β-actin(1:1000, Abcam, Cat#ab6276); Rabbit anti-Arginase-1 (1:1000, Cell Signaling Technology, Cat#93668).

    Techniques: Activation Assay, Activity Assay

    OGD/R injury with SalB or CBX application influenced astrocytic phosphorylated Cx43 and corresponding kinases. a1 , a2 OGD/R injury had no significant effect on cytoplasmic PKCε levels but significantly increased plasma membrane levels of PKCε and its Ser729-phosphorylated activated state. SalB and CBX reduced PKCε levels in the plasma membrane and increased them in the cytoplasm. Conversely, the OGD/R group’s Ser368-phosphorylated Cx43 levels were decreased in the plasma membrane and increased in the cytoplasm. SalB reversed these effects, but CBX reduced Ser368-phosphorylated Cx43 levels. b1 , b2 The OGD/R group exhibited decreased cytoplasmic levels of Thr308-phosphorylated PKB, though SalB reversed this effect. There were no significant changes in the plasma membrane levels. Furthermore, the OGD/R group exhibited elevated cytoplasmic and plasma membrane levels of Ser373-phosphorylated Cx43. SalB reduced the plasma membrane levels but further increased the cytoplasmic levels. CBX had little effect on the levels of Ser373-phosphorylated Cx43 and Thr308-phosphorylated PKB. c1 , c2 The OGD/R group exhibited elevated cytoplasmic and plasma membrane levels of Tyr416-phosphorylated Src. The OGD/R group also exhibited elevated plasma membrane levels of Src, which may be related to the elevated Tyr416-phosphorylated Src levels. SalB increased the plasma membrane levels of Src’s Tyr527-phosphorylated deactivated form but did not significantly affect plasma membrane levels of Tyr416-phosphorylated Src. CBX significantly reduced cytoplasmic and plasma membrane levels of Tyr416-phosphorylated Src. Furthermore, the OGD/R group exhibited increased cytoplasmic and plasma membrane levels of Tyr265-phosphorylated Cx43. SalB reversed this effect, but CBX achieved only non-significant reduction of the plasma membrane levels. We evaluated the statistical significance with ANOVA and Duncan’s multiple comparisons test. * p

    Journal: Journal of Neuroinflammation

    Article Title: Roles of astrocytic connexin-43, hemichannels, and gap junctions in oxygen-glucose deprivation/reperfusion injury induced neuroinflammation and the possible regulatory mechanisms of salvianolic acid B and carbenoxolone

    doi: 10.1186/s12974-018-1127-3

    Figure Lengend Snippet: OGD/R injury with SalB or CBX application influenced astrocytic phosphorylated Cx43 and corresponding kinases. a1 , a2 OGD/R injury had no significant effect on cytoplasmic PKCε levels but significantly increased plasma membrane levels of PKCε and its Ser729-phosphorylated activated state. SalB and CBX reduced PKCε levels in the plasma membrane and increased them in the cytoplasm. Conversely, the OGD/R group’s Ser368-phosphorylated Cx43 levels were decreased in the plasma membrane and increased in the cytoplasm. SalB reversed these effects, but CBX reduced Ser368-phosphorylated Cx43 levels. b1 , b2 The OGD/R group exhibited decreased cytoplasmic levels of Thr308-phosphorylated PKB, though SalB reversed this effect. There were no significant changes in the plasma membrane levels. Furthermore, the OGD/R group exhibited elevated cytoplasmic and plasma membrane levels of Ser373-phosphorylated Cx43. SalB reduced the plasma membrane levels but further increased the cytoplasmic levels. CBX had little effect on the levels of Ser373-phosphorylated Cx43 and Thr308-phosphorylated PKB. c1 , c2 The OGD/R group exhibited elevated cytoplasmic and plasma membrane levels of Tyr416-phosphorylated Src. The OGD/R group also exhibited elevated plasma membrane levels of Src, which may be related to the elevated Tyr416-phosphorylated Src levels. SalB increased the plasma membrane levels of Src’s Tyr527-phosphorylated deactivated form but did not significantly affect plasma membrane levels of Tyr416-phosphorylated Src. CBX significantly reduced cytoplasmic and plasma membrane levels of Tyr416-phosphorylated Src. Furthermore, the OGD/R group exhibited increased cytoplasmic and plasma membrane levels of Tyr265-phosphorylated Cx43. SalB reversed this effect, but CBX achieved only non-significant reduction of the plasma membrane levels. We evaluated the statistical significance with ANOVA and Duncan’s multiple comparisons test. * p

    Article Snippet: Western blot analysis Protein concentration was evaluated using the BCA method, and 20–40 μg of total extract was separated on SDS polyacrilamide gels, and then the gel-separated proteins were transferred onto polyvinylidene fluoride (PVDF) membranes and probed using the indicated primary antibodies: overnight at 4 °C with Rabbit anti-pan Cx43(1:1000, Cell signaling technology, Cat#3512); Rabbit anti-phospho-Cx43/ GJA1(Ser 368)(1:1000, Abcam,Cat#ab30559); Rabbit anti-phospho-Cx43 (Ser373) (1:1000, Thermo Fisher Scientific, Cat#PA5-64670); Rabbit anti-phospho-Cx43(Ser265)(1:500, Thermo Fisher Scientific, Cat#PA5-37584); Rabbit anti-PKCε (1:200, Santa Cruz Biotechnology, Cat#sc-214); Goat anti-phospho-PKCε (Ser729) (1: 200, Santa Cruz Biotechnology, Cat#sc-12355); Rabbit anti-Akt(PKB) (1:1000, Cell Signaling Technology, Cat#4691); Rabbit anti-phospho-Akt(Thr308) antibody (1:1000, Cell Signaling Technology, Cat#13038); Rabbit anti-Src (1:1000, Cell Signaling Technology, Cat#2108); Rabbit anti-Phospho-Src(Tyr527) (1:1000, Cell Signaling Technology, Cat#2105); Rabbit anti-Phospho-Src(Tyr416) (1:1000, Cell Signaling Technology, Cat#6943); Rabbit anti-GAPDH antibody (1/5000, Abcam, Cat#ab37168); mouse anti-β-actin(1:1000, Abcam, Cat#ab6276); Rabbit anti-Arginase-1 (1:1000, Cell Signaling Technology, Cat#93668).

    Techniques: