- 14-9523-82 - Invitrogen Antibodies GAPDHS antibody

Submitted references Melatonin Protects Against Ischemic Brain Injury by Modulating PI3K/AKT Signaling Pathway via Suppression of PTEN Activity.

Ran Y, Ye L, Ding Z, Gao F, Yang S, Fang B, Liu Z, Xi J
ASN neuro 2021 Jan-Dec;13:17590914211022888

Antitumor activity of the dual BET and CBP/EP300 inhibitor NEO2734.

Spriano F, Gaudio E, Cascione L, Tarantelli C, Melle F, Motta G, Priebe V, Rinaldi A, Golino G, Mensah AA, Aresu L, Zucca E, Pileri S, Witcher M, Brown B, Wahlestedt C, Giles F, Stathis A, Bertoni F
Blood advances 2020 Sep 8;4(17):4124-4135

Rap1 deficiency-provoked paracrine dysfunction impairs immunosuppressive potency of mesenchymal stem cells in allograft rejection of heart transplantation.

Ding Y, Liang X, Zhang Y, Yi L, Shum HC, Chen Q, Chan BP, Fan H, Liu Z, Tergaonkar V, Qi Z, Tse HF, Lian Q
Cell death & disease 2018 Mar 7;9(3):386

Phenotypic switch in lung interstitial macrophage polarization in an ovalbumin-induced mouse model of asthma.

Nie H, Wang A, He Q, Yang Q, Liu L, Zhang G, Huang Y, Ding X, Yu H, Hu S
Experimental and therapeutic medicine 2017 Aug;14(2):1284-1292

Ras-association domain family 10 acts as a novel tumor suppressor through modulating MMP2 in hepatocarcinoma.

Liu W, Wang J, Wang L, Qian C, Qian Y, Xuan H, Zhuo W, Li X, Yu J, Si J
Oncogenesis 2016 Jun 27;5(6):e237

The CXCL12/CXCR4 Signaling Pathway: A New Susceptibility Factor in Human Papillomavirus Pathogenesis.

Meuris F, Carthagena L, Jaracz-Ros A, Gaudin F, Cutolo P, Deback C, Xue Y, Thierry F, Doorbar J, Bachelerie F
PLoS pathogens 2016 Dec;12(12):e1006039

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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Immunoblotting of reduced HeLa cells using 5 µg/mL of Anti-Human GAPDH Purified antibody.Bands were visualized using Anti-Mouse IgG HRP.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Western blot analysis was performed on whole cell extracts (30 µg lysate) of A549 (Lane 1), MDA-MB-231 (Lane 2) and COS-7 (Lane 3). The blot was probed with Anti-GAPDH Monoclonal Antibody (Product # 14-9523-80, 1 µg/mL) and detected by chemiluminescence using Goat anti-Mouse IgG (H+L) Superclonal™ Secondary Antibody, HRP conjugate (Product # A28177, 0.25 µg/mL, 1:4000 dilution). A 37 kDa band corresponding to GAPDH was observed across the cell lines tested.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 3. Expression of Arg1, iNOS and IL-10 in lung IMs of OVA-induced asthmatic mice. Lung IMs from OVA-induced asthmatic mice and PBS-treated control mice were sorted 24 h after the final OVA challenge (day 27 post-model establishment; 100 ug in 50 ul PBS) and (A) western blot analysis was used to measure Arg1, IL-10 and iNOS protein expression. GAPDH was used as a protein loading control and images are representative of 6 mice in each group. ODs of (B) Arg1, (C) iNOS and (D) IL-10 levels normalized to GAPDH. Data are presented as the mean +- standard deviation, n=6. **P

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Fig 6 Normalizing beta-arrestin-dependent signaling of CXCR4 1013 partially restores the productive HPV life cycle. (A) Western blots (left) and densitometric analyses (right) showing relative levels of HPV18-E2 protein in HPV18-positive CXCR4 wt , CXCR4 1013 , and CXCR4 1013&DeltaSHSK raft cultures. E2 protein levels were normalized to GAPDH protein levels and arbitrarily set at 1 for CXCR4 wt rafts (staining controls are shown in S5 Fig ). Values are means +- SEM. **p < 0.01 and ***p < 0.001. HPV18-positive CXCR4 1013&DeltaSHSK raft sections stained for HPV18-E4 (B), HPV18-L1 (C), and Ki-67 (D) expression by immunohistochemical staining. Images are representative of three independent experiments. Scale bars = 100 mum, inset scale bar = 10 mum.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 3. Melatonin Treatment Significantly Improves Cell Survival via the Activation of PI3K/Akt Pathway After Ischemic Stroke In Vitro and In Vivo . A-F: In vitro , N2a cells were treated with 25 nM melatonin for 24 hours after OGD in the presence or absence of wortmannin. A: Cell survival. B: Evaluation of the purity of the cell membrane and cytoplasm isolation of N2a cells. Western blots analysis of the different protein markers sodium potassium ATPase (plasma membrane), GRP94 (endoplasmic reticulum), Ku86 (nuclear) and GAPDH (cytoplasm). C: Representative western blots of p-Akt and Akt in the membrane and cytoplasm fractions. Quantification of western blots data of Akt (D), p-Akt expression (E), p-Akt/Akt ratio (F), respectively. The data resulted from Figure 3C . Values are mean +- SEM. *** p < 0.001 vs . vehicle; ## p < 0.01, ### p < 0.001 vs . vehicle plus OGD; ++ p < 0.05, +++ p < 0.01 vs . vehicle plus OGD plus 25 nM melatonin. One-way ANOVA followed by Bonferroni post hoc test. Samples were collected from three independent experiments, each performed in duplicate. G-J: In vivo , mice were subjected to dMCAO and treated with 20 mg/kg melatonin at 72 hours after ischemic stroke. G: Representative western blots of p-Akt and Akt in mice. H: Quantification of Akt, p-Akt expression, and p-Akt/Akt ratio. The data resulted from Figure 3G . I: Representative co-immunostaining of p-Akt (red) and NeuN (green). Nuclei were labeled with DAPI (blue) in each group. Scale bar=50 u

14-9523-82

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