GAPDH Antibody | Affinity Biosciences

$Fig.2 NaAsO2 induced autophagy, activation of NLRP3 inflammasome and 662 hepatic stellate cell in vivo. (A) The expression level of LC3 and p62 in rat livers 663 following exposure to NaAsO2. The protein fraction was analyzed by Western blot. (B) 664 The expression level of cytoplasmic CTSB in rat livers following exposure to NaAsO2. 665 The protein fraction was analyzed by Western blot. (C) The expression level of NLRP3 inflammasome-associated proteins in rat livers following exposure to NaAsO2. 667 The protein fraction was analyzed by Western blot. (D) The expression level of 668 Collagen- , α-SMA, MMP-1, and TIMP-1in rat livers following exposure to NaAsO2. 669 The protein fraction was analyzed by Western blot. (E) α-SMA was detected by IF. 670 White arrows indicate positive staining. Values are mean ± SD, and n = 5. *p < 0.05, 671 **p < 0.01 compared with the control group; Scale bar = 100 µm$

Fig.

Figure 7.

Fig 4.

$Fig.2 The effect of NaAsO2 on mitophagy, ox-mtDNA and NLRP3 inflammation in rats liver. Male SD rats were treated with 2.5, 5 mg/kg of NaAsO2 for 3 months. Liver coefficient (A). The level of serum ALT and AST were determined by commercial reagent kits (B-C). H&E staining of liver sections after NaAsO2 administration (D). scale bar = 500 μm. NAS in rat liver (E). Cytosolic fractions were analyzed by Western blot analysis. GAPDH was used as an internal control. The relative expression of MPO was shown as the percentage of GAPDH (F-G). The level of oxmtDNA was measured with an ELISA kit (H). Mitochondria fractions were analyzed by Western blot analysis. VDAC1, mitochondria marker protein, was used as an Journal Pre-proof internal control. The protein level and densitometric analyses of PINK1, Parkin, LC3B in rats liver tissues (I-L). The protein level and densitometric analyses of NLRP3, IL-1β, IL-18 expressed in rat liver tissues (M-T). Results are mean ± SEM of 5 rats. *P < 0.05 compare with the control group.$

Fig.

Figure 5.

FIGURE 3 NaAsO2 caused activation of IRE1α–endoplasmic reticulum‐stress pathway, NOX4, and hepatic stellate cell in vitro.

Fig.

FIGURE 2 | RIPK1/RIPK3/MLKL-mediated necroptosis was involved in compression-induced death of NPSCs.

$Fig. 3 β-arr2 depletion enhances TLR4-mediated signaling in B lymphocytes of mice with CAIA. a The relative expression of β-arr2 in splenic B lymphocytes from WT control mice and WT mice with CAIA. The intensity of the Western blot bands was analyzed by ImageJ software. b Membrane TLR4 expression on B lymphocytes was detected by flow cytometry, and cells only labeled with secondary antibody were used as negative controls. c Cytoplasmic TLR4 expression was determined using cytosolic proteins extracted from B lymphocytes by ultracentrifugation, and ATP1A1 was used to evaluate the purity of the isolated cytosolic fractions. d The interaction between β-arr2 and TLR4 was assessed by immunofluorescence, and the colocalization rate (%) was analyzed using the built-in software of the confocal microscope. e The mean fluorescence intensity of NF-κB p65 in the nucleus was measured as an indicator of the activity of NF-κB. *P < 0.05, **P < 0.01, ***P < 0.001 (n = 5).$

Fig.

Figure 6 CeO2NPs modulate osteoclast-specific gene expression via up- or downregulating the MAPK pathway, NF-κB pathway, and Nfatc1 signaling in a concentrationdependent manner.

FIGURE 5 TRIM44 is a molecular target of miR-134.

Fig.

FIGURE 4 Ellagic acid promotes pulmonary fibroblast autophagy mainly via inhibiting Wnt-mTOR signaling pathway (A,B) Mlg cells were exposed to CQ (20 µM) and Baf A1 (100 nM) with or without Ellagic acid (5 µM, 10 µM) to analyze the p62 expression level by using western blot.

Figure 5.

Figure 10.

Fig.

Figure 5 | Endostatin inhibits the expressions of α-SMA, RhoA, and ROCK1 at protein level.

FIGURE 5 FMN inhibits myostatin-mediated dephosphorylation on the PI3K/Akt/FoxO3a signalling pathway in the muscle of CKD rats and C2C12 myotubes.

FIGURE 3 | Protein expression of α2NKA, α1NKA, and Kv3.

Fig.

Figure5|Anlotinib antagonizes TGF-b1-mediated Smad and non-Smad signalling.

Fig.

FIGURE 6 | Effects of Huangqin decoction (HQD) on colonic expression levels of Ras-phosphoinositide-3-kinase (PI3K)-Akt-hypoxia inducible factor 1 alpha (HIF-1a) pathway proteins assessed by Western blot in dextran sulfate sodium (DSS)-induced colitis mice (A).

$Fig. 3 Receptor–ligand interactions of compound. a Protocol flowchart of MYC inhibitor discovery strategy, ten candidate inhibitors including okanin were screened at last through HTV, SP,and XP screen methods. b Binding model of MYC–DNA complexes with okanin (PDB code: 1NKP) through molecular docking method.The results showed that okanin interacted with two key amino acid residues in the DNA binding site of MYC. c Okanin could significantly inhibit the transcriptional regulatory activity of MYC by luciferase assay. d Okanin significantly inhibited the expressions of GLUT2 and p65, which were the downstream proteins of MYC(n = 3, **P \0.01)$

Fig.

Figure 4.

Fig.

$Figure 6. |Effects of HICA on the protein synthesis and production of inflammatory proteins.The basal fractional protein synthesis rate (A); 3-MeHis concentration in the medium (B); relative expression of atrogin-1, MURF1, and iNOS (C–F); and IL-6 production (G) of vehicle- or HICA-treated myotubes under normal or cachexic conditions. The time course of this set of experiments is shown in the upper left region. GM: growth medium and DM: differentiation medium. A typical image for Western blotting is shown (C). V: vehicle and, H: HICA (C). A typical image for a capillary immunoassay is shown in the left panel (F).$

Figure 6.

Fig.

Figure 3.

Figure 3:| 1e effect of ARE on proapoptotic protein expression and MMP.

Figure 3.

Fig.

FIGURE 3|Effects of ABP on the protein expression of CYP7A1 and SREBP-1C in rat liver tissue.

Fig.

$FIGURE 5 | Feline and human BCA2 restrict HIV-1 transcription by preventing HIV-1-induced activation of NF-κB.. (B,C) Five million HEK293T cells were transfected with 5 µg of VR1012, hBCA2, fBCA2, hBCA2 CA, or fBCA2 CA. After 48 h, cytoplasmic and nuclear fractions were separated and analyzed by western blotting to evaluate NF-κB 1(p105/p50), NF-κB p65, BCA2, GAPDH, and Histone H3 in each fraction. Results of quantitative band scan analysis of NF-κB p50/p65 were shown below, and the percentage of VR1012 quantifications are set to 100%.$

FIGURE 5 | Feline and human BCA2 restrict HIV-1 transcription by preventing HIV-1-induced activation of NF-κB.

FIGURE 1|Byakangelicin treatment reduces carbon tetrachloride-induced liver fibrosis.

FIGURE 2|FKN promoted the viability of J774A.

Figure 3.

Figure 2.

FIGURE 4 | Ellagic acid promotes pulmonary fibroblast autophagy mainly via inhibiting Wnt-mTOR signaling pathway (A,B) Mlg cells were exposed to CQ (20 µM) and Baf A1 (100 nM) with or without Ellagic acid (5 µM, 10 µM) to analyze the p62 expression level by using western blot.

Figure 6: |MEL attenuated the protein levels of NLRP3, TLR4, NF-κB, and caspase-1 of the terminal ileum tissues in NEC mice.

Figure 4:| TT inhibited the inflammatory activation of microglia and astrocytes.

FIGURE 13| Validation of regulated signalling pathways, spermatogenic cell apoptosis and proliferation, and meiotic spermatocytes by Western blot.

FIGURE s4 |The total proteins of infected primary peritoneal macrophages were extracted at 24, 36, 48, and 72 h post-infection and then subjected for Western blotting.

Figure 1.

Figure 7 |: Effect of downregulating miR-128 on the PIK3R1/Akt/mTOR pathway.

Figure S4|.

Fig.

Figure 6 |The effect of sevoflurane on the protein expression of p53 and Nrf2 in liver tissue induced by IR.

Figure 9 Effects of emodin on VEGF-A expression in MCAO rats.

Figure 7 A DAPK1 inhibitor prevents the PTBP1 knockdown induced reprogramming.

FIGURE 5 miR-200a-3p directly targets the 3′UTR of MAPK14 and regulates the expression levels of p38, c-jun, ET-1 and VEGFA.

Figure 9 IF-C2C12 Exos down-regulated C2C12 fibrogenic/myogenic differentiation-related proteins in vitro.

Fig.

Figure 2 Mitophagy decreases with the activation of HSCs, and MitoQ enhances mitophagy.

Figure 6 Tuina treatment influenced the expression of pyroptosis-related molecules in the hippocampi of HIE rats.

Fig.

FIGURE 7 The expression of HIF-1α and HIF-2α in the brain was increased in the HDM group.

FIGURE 1 ECM stiffness activates MCs.

FIGURE 2 CircNFIX maintained hADSC chondrogenesis and prevented chondrocyte degeneration.

Figure 5 Prdm16 and Ucp-1 expression in subcutaneous WAT and comparison of serum leptin levels in each group.

Figure 4 Puerarin treatment activates cell apoptosis and related proteins, while suppressing IL-6, TNF-α, and CA125 levels and modulating CD3+CD4+CD3+/CD8+ T lymphocyte percentages in OC tumor-bearing Fischer 344 rats.

Figure 1.

FIGURE 5 Evodiamine exerts anti-inflammatory effects in OA by modulating the NF-κB pathway.

Figure 3 Inhibitory effect of rhein on SHH signaling pathway in UUO rats.

Fig.

Figure 7 JP can increase FXR expression to suppress α-SMA expression at the transcriptional and protein levels.

Fig.

FIGURE 3 Umbelliferone and scopoletin differentially inhibited RA-FLS activities.

FIGURE 3 mRNA and protein expression of ABCA12 in pancreatic cancer.

FIGURE 5 Transcription factor p53 regulates ARHGAP24 gene expression in porcine neural cells.

Figure 5 Effects of DOP treatment on the PI3K–Akt–mTOR signaling pathway in rats by qPCR and Western blot.

Figure 8 Expression of PI3K/Akt/GSK-3β pathway-related proteins in FHC (a) and IEC-6 (b) cells.

Figure 3 ACTN4 targets on miR-125a-3p via TP73-AS1.

Figure 2 The expression level of chemokines, adhesion molecules, and KLF6 expression in histamine-treated hNECs were repressed by febuxostat.

Fig.

Figure 8 The effect of OBB on the MAPK signaling pathway in 5-FU-induced IM mice.

FIGURE 2 FG‐4592 inhibits apoptosis and promotes autophagy in bone marrow stromal cell (BMSC) post‐oxygen–glucose deprivation (OGD).

FIGURE 7 Deoxycholic acid (DCA) accelerated vasculogenic mimicry formation, epithelial‐mesenchymal transition, and migration in HCT‐116 cells.

Fig.

Figure 6 Importance of VDR in calcitriol-regulated inflammatory cytokines expressions.

Figure 6 The effect of sevoflurane on the protein expression of p53 and Nrf2 in liver tissue induced by IR.

FIGURE 3 Effect of ROF on CYP2E1 protein and TLR4/NF-κB axis in mice.

4 小鼠卵巢颗粒细胞中p-PI3K、PI3K、p-Akt及Akt蛋白表达情况 Protein expression of p-PI3K, PI3K, p-Akt, and Akt in ovarian granulosa cells in different groups (Mean±SD, n=3).

Figure 7 Effect of JXD on the cell apoptosis in pulmonary tissue of BLM-induced PF rats.

Fig.

Figure 3 EPO regulates the expression of ferroptotic biomarkers after SCI.

Figure 6 EO regulated Akt/p38 MAPK pathway-related proteins in human TNBC cells.

Figure 5 KRT17 regulates LSCC progression by affecting AKT/mTOR and Wnt/β-catenin axes (a).

Figure 3 The effect of tumor-derived exosomes on pancreatic cancer (PC) on the xenograft tumor model.

Figure 8 Knockdown of LAMC2 reduced the expression of LAMC2, Ki-67, and integrinβ1, while increased the expression of E-cadherin.

Figure 9 APL extract inhibited cardiomyocyte apoptosis of Iso-induced mice.

FIGURE 2 Licoricidin promoted MGC-803 cell apoptosis and arrested mitosis in the G0/G1 phase.

Figure 6 Effects of GA on Keap1-Nrf2 signaling.

Figure 5 The expression degrees of HMGB1, TLR4, NF-κB, p-38 MAPK, and ERK1/2 proteins (x¯ ±s).

Fig.

Figure 10 The expressions of cleaved caspase 1/caspase 1 and cleaved caspase 3/caspase 3 in lung tissues were detected by western blot.

Figure 8 Storax inhibits the AT1R–Ankrd1–P53 pathway in AMI rats against cardiomyocyte apoptosis.

Fig.

Figure 4 The impact of C/EBPα in angiotensin II- (Ang II-) treated VSMCs.

Figure 4 Estrogen deficiency exacerbates hippocampal neuron loss in mice.

Figure 4 Effects of FV on liver lipogenesis-related markers in the mice fed with HFD.

Figure 7 Sal B and Gom D attenuate HSCs activation via PDGFRβ pathway.

Fig.

Figure 2 miR-22-5p regulates NSCLC cell proliferation, migration, invasion, and EMT.

Figure 3.

Figure 2.

Figure 5 Circ_0007611 mediated IL1RAP expression through miR-558.

Fig.

Product:	GAPDH Antibody
Catalog:	AF7021
Description:	Rabbit polyclonal antibody to GAPDH
Application:	WB IHC IF/ICC
Reactivity:	Human, Mouse, Rat, Pig, Bovine, Goat, Monkey, Chicken
Prediction:	Pig, Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
Mol.Wt.:	37kDa; 36kD(Calculated).
Uniprot:	P04406
RRID:	AB_2839421

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Blocking peptides are peptides that bind specifically to the target antibody and block antibody binding. These peptide usually contains the epitope recognized by the antibody. Antibodies bound to the blocking peptide no longer bind to the epitope on the target protein. By comparing the staining from the blocked antibody versus the antibody alone, one can see which staining is specific.

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Product Info

Source:

Rabbit

Application:

WB 1:3000-1:30000, IHC 1:50-1:200, IF/ICC 1:200
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:

Human,Mouse,Rat,Pig,Bovine,Goat,Monkey,Chicken

Prediction:

Horse(100%), Sheep(100%), Rabbit(100%), Dog(100%), Xenopus(90%)

Clonality:

Polyclonal

Specificity:

GAPDH antibody detects endogenous levels of total GAPDH.

RRID:

AB_2839421
Cite Format: Affinity Biosciences Cat# AF7021, RRID:AB_2839421.

Conjugate:

Unconjugated.

Purification:

The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).

Storage:

Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.

Alias:

Fold/Unfold

GAPDH, A1 40 kd subunit, Activator 1 40 kd subunit, G3PD, GAPD, G3pdh, Rfc40, Rf-c 40 kd subunit

Immunogens

Immunogen:

A synthesized peptide derived from human GAPDH.

Uniprot:

P04406(G3P_HUMAN) >>Visit HPA database.

Gene(ID):

GAPDH(2597)

Description:

Glyceraldehyde 3 phosphate dehydrogenase (GAPDH) iswell known as one of the key enzymes involved in glycolysis.As well as functioning as a glycolytic enzyme in cytoplasm,recent evidence suggests that mammalian GAPDHis also involved in a great number of intracellular procesessuch as membrane fusion, microtubule bundling, phosphotransferaseactivity, nuclear RNA export, DNA replication,and DNA repair.

Sequence:

P04406 G3P_HUMAN:
Protein BLAST With
NCBI/
ExPASy/
Uniprot

MGKVKVGVNGFGRIGRLVTRAAFNSGKVDIVAINDPFIDLNYMVYMFQYDSTHGKFHGTVKAENGKLVINGNPITIFQERDPSKIKWGDAGAEYVVESTGVFTTMEKAGAHLQGGAKRVIISAPSADAPMFVMGVNHEKYDNSLKIISNASCTTNCLAPLAKVIHDNFGIVEGLMTTVHAITATQKTVDGPSGKLWRDGRGALQNIIPASTGAAKAVGKVIPELNGKLTGMAFRVPTANVSVVDLTCRLEKPAKYDDIKKVVKQASEGPLKGILGYTEHQVVSSDFNSDTHSSTFDAGAGIALNDHFVKLISWYDNEFGYSNRVVDLMAHMASKE

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species

Results

Score

Pig

100

Horse

100

Bovine

100

Sheep

100

Dog

100

Chicken

100

Rabbit

100

Xenopus

Zebrafish

Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

Research Backgrounds

P04406_G3P_HUMAN

Function:

Has both glyceraldehyde-3-phosphate dehydrogenase and nitrosylase activities, thereby playing a role in glycolysis and nuclear functions, respectively. Participates in nuclear events including transcription, RNA transport, DNA replication and apoptosis. Nuclear functions are probably due to the nitrosylase activity that mediates cysteine S-nitrosylation of nuclear target proteins such as SIRT1, HDAC2 and PRKDC. Modulates the organization and assembly of the cytoskeleton. Facilitates the CHP1-dependent microtubule and membrane associations through its ability to stimulate the binding of CHP1 to microtubules (By similarity). Glyceraldehyde-3-phosphate dehydrogenase is a key enzyme in glycolysis that catalyzes the first step of the pathway by converting D-glyceraldehyde 3-phosphate (G3P) into 3-phospho-D-glyceroyl phosphate. Component of the GAIT (gamma interferon-activated inhibitor of translation) complex which mediates interferon-gamma-induced transcript-selective translation inhibition in inflammation processes. Upon interferon-gamma treatment assembles into the GAIT complex which binds to stem loop-containing GAIT elements in the 3'-UTR of diverse inflammatory mRNAs (such as ceruplasmin) and suppresses their translation.

PTMs:

S-nitrosylation of Cys-152 leads to interaction with SIAH1, followed by translocation to the nucleus (By similarity). S-nitrosylation of Cys-247 is induced by interferon-gamma and LDL(ox) implicating the iNOS-S100A8/9 transnitrosylase complex and seems to prevent interaction with phosphorylated RPL13A and to interfere with GAIT complex activity.

ISGylated.

Sulfhydration at Cys-152 increases catalytic activity.

Oxidative stress can promote the formation of high molecular weight disulfide-linked GAPDH aggregates, through a process called nucleocytoplasmic coagulation. Such aggregates can be observed in vivo in the affected tissues of patients with Alzheimer disease or alcoholic liver cirrhosis, or in cell cultures during necrosis. Oxidation at Met-46 may play a pivotal role in the formation of these insoluble structures. This modification has been detected in vitro following treatment with free radical donor (+/-)-(E)-4-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexenamide. It has been proposed to destabilize nearby residues, increasing the likelihood of secondary oxidative damages, including oxidation of Tyr-45 and Met-105. This cascade of oxidations may augment GAPDH misfolding, leading to intermolecular disulfide cross-linking and aggregation.

Succination of Cys-152 and Cys-247 by the Krebs cycle intermediate fumarate, which leads to S-(2-succinyl)cysteine residues, inhibits glyceraldehyde-3-phosphate dehydrogenase activity. Fumarate concentration as well as succination of cysteine residues in GAPDH is significantly increased in muscle of diabetic mammals. It was proposed that the S-(2-succinyl)cysteine chemical modification may be a useful biomarker of mitochondrial and oxidative stress in diabetes and that succination of GAPDH and other thiol proteins by fumarate may contribute to the metabolic changes underlying the development of diabetes complications.

Subcellular Location:

Cytoplasm>Cytosol. Nucleus. Cytoplasm>Perinuclear region. Membrane. Cytoplasm>Cytoskeleton.
Note: Translocates to the nucleus following S-nitrosylation and interaction with SIAH1, which contains a nuclear localization signal (By similarity). Postnuclear and Perinuclear regions.

Subunit Structure:

Homotetramer. Interacts with TPPP; the interaction is direct. Interacts (when S-nitrosylated) with SIAH1; leading to nuclear translocation. Interacts with RILPL1/GOSPEL, leading to prevent the interaction between GAPDH and SIAH1 and prevent nuclear translocation. Interacts with CHP1; the interaction increases the binding of CHP1 with microtubules. Associates with microtubules (By similarity). Interacts with EIF1AD, USP25, PRKCI and WARS1. Interacts with phosphorylated RPL13A; inhibited by oxidatively-modified low-densitity lipoprotein (LDL(ox)). Component of the GAIT complex. Interacts with FKBP6; leading to inhibit GAPDH catalytic activity.

Family&Domains:

The [IL]-x-C-x-x-[DE] motif is a proposed target motif for cysteine S-nitrosylation mediated by the iNOS-S100A8/A9 transnitrosylase complex.

Belongs to the glyceraldehyde-3-phosphate dehydrogenase family.

Research Fields

· Environmental Information Processing > Signal transduction > HIF-1 signaling pathway. (View pathway)

· Human Diseases > Neurodegenerative diseases > Alzheimer's disease.

· Metabolism > Carbohydrate metabolism > Glycolysis / Gluconeogenesis.

· Metabolism > Global and overview maps > Metabolic pathways.

· Metabolism > Global and overview maps > Carbon metabolism.

· Metabolism > Global and overview maps > Biosynthesis of amino acids.

References

1). Large-scale generation of functional mRNA-encapsulating exosomes via cellular nanoporation. Nature Biomedical Engineering (PubMed: 31844155) [IF=28.1]

Application: WB Species: Mice Sample: Tumour cells

Fig. 5 | CNP increases exosome release through HSP–p53–TASP6 signalling pathway. a, Simulated temperature changes at five selected locations. A 200 V and 10 ms pulse created a localized ‘hot spot’ in the nanochannel outlet with a power density of ~1 × 1014 W m−3 and a peak temperature up to 60 °C from room temperature. Once the pulse ended, the hot spot vanished rapidly due to the extremely small volume of the heated fluid inside the nanochannel (~1 × 10−12 cm3 ) compared with the bulk solution outside the nanochannel (~0.1 cm3 ). b, Top-down images of MEFs (green) attaching to the surface of the CNP device. Red dots show nanochannel locations and room temperature before CNP transfection (0 s). White arrows indicate locations of the nanochannels. The CNP electric pulse (CNP) sharply increases temperature at the nanochannel–cell surface interface. c, Cross-section view of nanochannels shows temperature changes in the nanochannels before (0 s), during and after (1 s) a CNP pulse. d, Temperature at the cell–nanochannel interface transiently (<1 s) increases to ~60 °C. e, Western blot of HSP90 and HSP70 from untreated (PBS) and CNP (with PBS)-stimulated (CNP) MEFs. f, DLS measurements of exosome concentrations from 108 CNP-stimulated MEFs with or without HSP inhibitors show that HSP70 and HSP90 are critical for the production of exosomes. NVP-HSP990, HSP90 inhibitor; VER155008, HSP70 inhibitor. g, Western blots show that CNP increases expression of p53 and TSAP6 protein in p53 wild-type MEFs, but does not affect p53 or TSAP6 protein expression in p53−/− MEFs. h, DLS measurements of exosome concentrations show that knockdown of p53 can partially block exosome release after CNP. i, Schematic of a proposed mechanism for CNP triggering of exosome release in CNP-transfected cells. Data are from three independent experiments and are presented as mean ± s.e.m. Two-sided Student’s t-test was used for the comparison.

2). In situ MUC1-specific CAR engineering of tumor-supportive macrophages stimulates tumoricidal immunity against pancreatic adenocarcinoma. Nano Today [IF=17.4]

3). Macrophage-tumor chimeric exosomes accumulate in lymph node and tumor to activate the immune response and the tumor microenvironment. Science Translational Medicine (PubMed: 34644149) [IF=17.1]

4). CXCL13/CXCR5 Signaling Contributes to Diabetes-induced Tactile Allodynia via Activating pERK, pSTAT3, pAKT Pathways and Pro-inflammatory Cytokines Production in the Spinal Cord of male mice. BRAIN BEHAVIOR AND IMMUNITY (PubMed: 31100371) [IF=15.1]

Application: WB Species: mouse Sample: spinal cord

Fig. 8.| (A) Comparison of mechanical threshold in WT group, db/db control group and db/db + U0126 administration group. The mechanical pain threshold was lower than those in the WT group. The mechanical pain threshold in the db/db + U0126 group were higher than those in the db/db control group. *** P < 0.001 vs WT mice; ## P < 0.01 vs db/db mice at the same age, Two-Way ANOVA with Bonferroni’s post hoc test, n = 6 mice per group. (B-G) Analysis protein expression levels in the spinal cord of the db/db control group and the db/db + U0126 administration group. * P < 0.05 vs db/db mice at the same age, Student’s t test, n = 3mice per group.

5). Extracellular vesicles derived from human dermal fibroblast effectively ameliorate skin photoaging via miRNA-22-5p-GDF11 axis. Chemical Engineering Journal [IF=15.1]

6). Identification of anthelmintic parbendazole as a therapeutic molecule for HNSCC through connectivity map-based drug repositioning. Acta Pharmaceutica Sinica B (PubMed: 35646536) [IF=14.5]

7). In situ synthesis and unidirectional insertion of membrane proteins in liposome-immobilized silica stationary phase for rapid preparation of microaffinity chromatography. Acta Pharmaceutica Sinica B (PubMed: 36176904) [IF=14.5]

Application: WB Species: Rat Sample: HSC-T6 cells

Figure 7 Sal B and Gom D attenuate HSCs activation via PDGFRβ pathway. The mRNA levels of α-SMA (A) and collagen Ӏ (B) in HSC-T6 cells treated with Sal B and Gom D, n = 3–4. (C, D) The effect of siRNA PDGFRβ on Sal B and Gom D′ inhibition in HSC-T6 cellular activation, n = 4–5. The protein levels associated PDGFRβ pathway in HSC-T6 cells treated with Sal B (E) and Gom D (F), n = 3. Data are shown as mean ± SD. ∗∗P < 0.01, ∗∗∗P < 0.001 versus control group; #P < 0.05, ##P < 0.01, ###P < 0.001 versus TGF-β group. $$$P < 0.001 versus siRNA PDGFRβ-Control group.

8). Gold nanoparticles targeting the autophagy–lysosome system to combat the inflammation-compromised osteogenic potential of periodontal ligament stem cells: From mechanism to therapy. Biomaterials (PubMed: 36030103) [IF=14.0]

9). Arsenic induces pancreatic dysfunction and ferroptosis via mitochondrial ROS-autophagy-lysosomal pathway. JOURNAL OF HAZARDOUS MATERIALS (PubMed: 31735470) [IF=13.6]

Application: WB Species: Rat Sample: MIN6 cells

Fig. 6 Ferroptosis was triggered by MtROS-dependent autophagy. (A) Effects of NaAsO2 (4  and TEMPO on LC3 and p62 in MIN6 cells. (B) Autophagic flux analysis. (C) The efficiency of CQ, and its effect on GPX4 and COX-2 in NaAsO2- Journal Pre-proof treated MIN6 cells. (D) Effects of NaAsO2 and CQ on relative GSH, T-SOD, and MDA content in MIN6 cells. (E) Effects of CQ on the NaAsO2-induced accumulation of lipid ROS by BODIPY 581/591 C11 staining (scale bar = 50 m). (F) Effects of CQ on the NaAsO2-induced insulin released using an ELISA kit. All results are expressed as the mean ± SD, n = 3. *P < 0.05, **P < 0.001 vs. control group, #P < 0.05, ##P < 0.001 vs. NaAsO2 group.

10). Arsenic induces hepatic insulin resistance via mtROS-NLRP3 inflammasome pathway. JOURNAL OF HAZARDOUS MATERIALS (PubMed: 32544768) [IF=13.6]

Application: WB Species: rat Sample: liver

Fig.2 The effect of NaAsO2 on mitophagy, ox-mtDNA and NLRP3 inflammation in rats liver. Male SD rats were treated with 2.5, 5 mg/kg of NaAsO2 for 3 months. Liver coefficient (A). The level of serum ALT and AST were determined by commercial reagent kits (B-C). H&E staining of liver sections after NaAsO2 administration (D). scale bar = 500 μm. NAS in rat liver (E). Cytosolic fractions were analyzed by Western blot analysis. GAPDH was used as an internal control. The relative expression of MPO was shown as the percentage of GAPDH (F-G). The level of oxmtDNA was measured with an ELISA kit (H). Mitochondria fractions were analyzed by Western blot analysis. VDAC1, mitochondria marker protein, was used as an Journal Pre-proof internal control. The protein level and densitometric analyses of PINK1, Parkin, LC3B in rats liver tissues (I-L). The protein level and densitometric analyses of NLRP3, IL-1β, IL-18 expressed in rat liver tissues (M-T). Results are mean ± SEM of 5 rats. *P < 0.05 compare with the control group.

Restrictive clause

Affinity Biosciences tests all products strictly. Citations are provided as a resource for additional applications that have not been validated by Affinity Biosciences. Please choose the appropriate format for each application and consult Materials and Methods sections for additional details about the use of any product in these publications.

For Research Use Only.
Not for use in diagnostic or therapeutic procedures. Not for resale. Not for distribution without written consent. Affinity Biosciences will not be held responsible for patent infringement or other violations that may occur with the use of our products. Affinity Biosciences, Affinity Biosciences Logo and all other trademarks are the property of Affinity Biosciences LTD.

GAPDH Antibody - #AF7021

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Related Downloads

MSDS

Data Sheet

COA

Protocols

WB Handbook

IHC Protocol

IF/ICC Protocol

Product Info

Immunogens

Predictions

Research Backgrounds

Research Fields

References

Restrictive clause