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glut 1 rabbit mab  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc glut 1 rabbit mab
    Glut 1 Rabbit Mab, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 90 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+glut+1/Glut1+Rabbit+mAb/pm41916290-299-19-22
    Average 95 stars, based on 90 article reviews
    glut 1 rabbit mab - by Bioz Stars, 2026-09
    95/100 stars

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    Related Articles

    other:

    Article Title: The type 2 cytokine Fc-IL-4 revitalizes exhausted CD8 + T cells against cancer.
    Article Snippet: Anti-rabbit HRP-IgG (7074) and anti-Glut-1 (73015) were purchased from Cell Signalling Technology.

    Article Title: Potent and selective chemical probe of hypoxic signalling downstream of HIF-α hydroxylation via VHL inhibition
    Article Snippet: Primary antibodies were used at following dilutions for CTLs: anti-HIF-1α (R&D; MAB1536; 1:500), anti-GLUT-1 (Cell Signaling Techonology; CS 129395; 1:1,000) and anti-SMC1 (Bethyl Laboratories, Inc.; A300-055A 1: 10,000).

    Article Title: Potent and selective chemical probe of hypoxic signalling downstream of HIF-α hydroxylation via VHL inhibition.
    Article Snippet: Primary antibodies were used at following dilutions for CTLs: anti-HIF-1a (R&D; MAB1536; 1:500), anti-GLUT-1 (Cell Signaling Techonology; CS 129395; 1:1,000) and anti-SMC1 (Bethyl Laboratories, Inc.; A300-055A 1: 10,000).

    Article Title: Potent and selective chemical probe of hypoxic signalling downstream of HIF-α hydroxylation via VHL inhibition.
    Article Snippet: Primary antibodies were used at following dilutions for mammalian cells: anti-HIF-1a (BD Biosciences; 610958; 1:1,000), anti-hydroxy-HIF-1a (Hyp564) (Cell Signaling Techonology; #3434; 1:1,000), anti-HIF-2a (R&D; AF 2886; 1:1,000), anti-CA9 (Novus Biologicals; NB100-417; 1:1,000), anti-GLUT-1 (Cell Signaling Techonology; CS 129395; 1:1000), anti-PHD2 (Bethyl Laboratories; A300-322A; 1:1,000), anti-PHD3 (Bethyl Laboratories; A300-327A; 1:1,000), anti-BNIP3 (abcam; ab10433; 1:10,000), anti-VHL (Cell Signaling Techonology; #2738; 1:1,000) anti-b-actin (Cell Signaling Techonology; #3700s; 1:10,000).

    Article Title: The type 2 cytokine Fc–IL-4 revitalizes exhausted CD8 + T cells against cancer
    Article Snippet: Anti-rabbit HRP-IgG (7074) and anti-Glut-1 (73015) were purchased from Cell Signalling Technology.

    Article Title: Potent and selective chemical probe of hypoxic signalling downstream of HIF-α hydroxylation via VHL inhibition
    Article Snippet: Primary antibodies were used at following dilutions for mammalian cells: anti-HIF-1α (BD Biosciences; 610958; 1:1,000), anti-hydroxy-HIF-1α (Hyp564) (Cell Signaling Techonology; #3434; 1:1,000), anti-HIF-2α (R&D; AF 2886; 1:1,000), anti-CA9 (Novus Biologicals; NB100-417; 1:1,000), anti-GLUT-1 (Cell Signaling Techonology; CS 129395; 1:1000), anti-PHD2 (Bethyl Laboratories; A300-322A; 1:1,000), anti-PHD3 (Bethyl Laboratories; A300-327A; 1:1,000), anti-BNIP3 (abcam; ab10433; 1:10,000), anti-VHL (Cell Signaling Techonology; #2738; 1:1,000) anti-β-actin (Cell Signaling Techonology; #3700s; 1:10,000).

    Incubation:

    Article Title: Regulatory interaction between metabolite transporters coordinates glucose and exometabolite fluxes to drive bioenergetics.
    Article Snippet: .. Next, the samples were incubated with anti-NaCT (Santa Cruz Biotechnology, Dallas, TX) diluted at 1:25 and anti-Glut-1 (Cell Signaling) diluted at 1:50 for 1 h at RT. .. After 3 wash cycles with PBST (0.1% Triton X 100 in PBS), the samples were incubated with Alexa 488 conjugated donkey antimouse and Cy3-conjugated donkey anti-rabbit antibodies (Jackson Immunoresearch Inc.) for 1 h at RT.



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    CAFs regulated the occurrence and development of CCA by activating the AKR1C3/STAT3 signaling axis. (A) The mRNA expression levels of AKR1C3 in QBC939 and TFK1 cells after co-incubation with CAFs were detected by Q-PCR. ** P < 0.01. (B) The protein expression levels of AKR1C3, P-STAT3, and T-STAT3 in QBC939 cells after co-incubation with CAFs at different times were measured by Western blot. (C) After CAF treatment with or without Ab-IL-6 and (or) AKR1C3 knockdown for 8 h, the expression of AKR1C3, P-STAT3, and T-STAT3 were detected by Western blot in QBC939 cells. (D) After treatment of CAFs with or without Ab-IL-6 and (or) AKR1C3 knockdown for 8 h, the expression of PCNA, P-GP, <t>GLUT-1,</t> and PFK-1 were detected by Western blot in QBC939 cells. The proliferation (E) and glycolysis levels (F) in QBC939 and TFK1 cells after treatment of CAFs with or without Ab-IL-6 and (or) AKR1C3 knockdown were assessed by CCK-8, glucose uptake, and lactate release, respectively. * P < 0.05, ** P < 0.01, *** P < 0.001. The cell colony (G) of QBC939 cells exposed to 40 µM 5-FU after treatment of CAFs with or without Ab-IL-6 and (or) AKR1C3 knockdown were detected by crystal violet staining. Ab-IL-6, 2ug/ml.
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    Image Search Results


    CAFs regulated the occurrence and development of CCA by activating the AKR1C3/STAT3 signaling axis. (A) The mRNA expression levels of AKR1C3 in QBC939 and TFK1 cells after co-incubation with CAFs were detected by Q-PCR. ** P < 0.01. (B) The protein expression levels of AKR1C3, P-STAT3, and T-STAT3 in QBC939 cells after co-incubation with CAFs at different times were measured by Western blot. (C) After CAF treatment with or without Ab-IL-6 and (or) AKR1C3 knockdown for 8 h, the expression of AKR1C3, P-STAT3, and T-STAT3 were detected by Western blot in QBC939 cells. (D) After treatment of CAFs with or without Ab-IL-6 and (or) AKR1C3 knockdown for 8 h, the expression of PCNA, P-GP, GLUT-1, and PFK-1 were detected by Western blot in QBC939 cells. The proliferation (E) and glycolysis levels (F) in QBC939 and TFK1 cells after treatment of CAFs with or without Ab-IL-6 and (or) AKR1C3 knockdown were assessed by CCK-8, glucose uptake, and lactate release, respectively. * P < 0.05, ** P < 0.01, *** P < 0.001. The cell colony (G) of QBC939 cells exposed to 40 µM 5-FU after treatment of CAFs with or without Ab-IL-6 and (or) AKR1C3 knockdown were detected by crystal violet staining. Ab-IL-6, 2ug/ml.

    Journal: Scientific Reports

    Article Title: Cancer-Associated fibroblasts regulate the development of cholangiocarcinoma through IL-6/STAT3/AKR1C3 signaling axis

    doi: 10.1038/s41598-026-37583-y

    Figure Lengend Snippet: CAFs regulated the occurrence and development of CCA by activating the AKR1C3/STAT3 signaling axis. (A) The mRNA expression levels of AKR1C3 in QBC939 and TFK1 cells after co-incubation with CAFs were detected by Q-PCR. ** P < 0.01. (B) The protein expression levels of AKR1C3, P-STAT3, and T-STAT3 in QBC939 cells after co-incubation with CAFs at different times were measured by Western blot. (C) After CAF treatment with or without Ab-IL-6 and (or) AKR1C3 knockdown for 8 h, the expression of AKR1C3, P-STAT3, and T-STAT3 were detected by Western blot in QBC939 cells. (D) After treatment of CAFs with or without Ab-IL-6 and (or) AKR1C3 knockdown for 8 h, the expression of PCNA, P-GP, GLUT-1, and PFK-1 were detected by Western blot in QBC939 cells. The proliferation (E) and glycolysis levels (F) in QBC939 and TFK1 cells after treatment of CAFs with or without Ab-IL-6 and (or) AKR1C3 knockdown were assessed by CCK-8, glucose uptake, and lactate release, respectively. * P < 0.05, ** P < 0.01, *** P < 0.001. The cell colony (G) of QBC939 cells exposed to 40 µM 5-FU after treatment of CAFs with or without Ab-IL-6 and (or) AKR1C3 knockdown were detected by crystal violet staining. Ab-IL-6, 2ug/ml.

    Article Snippet: Antibodies against P-STAT3 (9145 S), T-STAT3 (30835 S), PCNA (2586 S), P-GP (13879 S), GLUT-1 (73015 S) were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Expressing, Incubation, Western Blot, Knockdown, CCK-8 Assay, Staining

    CAFs regulated the occurrence and development of CCA via the IL-6/STAT3/AKR1C3 signaling axis in vivo. (A) shAKR1C3-QBC939 cells and control cells were subcutaneously injected in nude mice to establish xenograft tumors. The representative tumors and their volume are depicted graphically. (B) The growth and sensitivity to 5-FU were detected in the mixed xenografts of CAFs and shAKR1C3-QBC939 cells. (C) HE and IHC staining were performed to examine CAF-QBC939 and QBC939 xenografts. (D) The protein expressions of AKR1C3, P-STAT3, PCNA, P-GP, GLUT-1, and PFK-1 in the CAFs-shAKR1C3-QBC939 xenografts with or without the treatment of 5-FU were detected by Western blot. (E) Schematic summary illustrating how CAF-derived IL-6 activates the STAT3/AKR1C3 axis in cholangiocarcinoma cells to drive tumor proliferation, chemoresistance, glycolysis, and metastatic potential.

    Journal: Scientific Reports

    Article Title: Cancer-Associated fibroblasts regulate the development of cholangiocarcinoma through IL-6/STAT3/AKR1C3 signaling axis

    doi: 10.1038/s41598-026-37583-y

    Figure Lengend Snippet: CAFs regulated the occurrence and development of CCA via the IL-6/STAT3/AKR1C3 signaling axis in vivo. (A) shAKR1C3-QBC939 cells and control cells were subcutaneously injected in nude mice to establish xenograft tumors. The representative tumors and their volume are depicted graphically. (B) The growth and sensitivity to 5-FU were detected in the mixed xenografts of CAFs and shAKR1C3-QBC939 cells. (C) HE and IHC staining were performed to examine CAF-QBC939 and QBC939 xenografts. (D) The protein expressions of AKR1C3, P-STAT3, PCNA, P-GP, GLUT-1, and PFK-1 in the CAFs-shAKR1C3-QBC939 xenografts with or without the treatment of 5-FU were detected by Western blot. (E) Schematic summary illustrating how CAF-derived IL-6 activates the STAT3/AKR1C3 axis in cholangiocarcinoma cells to drive tumor proliferation, chemoresistance, glycolysis, and metastatic potential.

    Article Snippet: Antibodies against P-STAT3 (9145 S), T-STAT3 (30835 S), PCNA (2586 S), P-GP (13879 S), GLUT-1 (73015 S) were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: In Vivo, Control, Injection, Immunohistochemistry, Western Blot, Derivative Assay