Journal: Journal of cellular physiology

Article Title: Mitogen-Dependent Regulation of DUSP1 Governs ERK and p38 Signaling During Early 3T3-L1 Adipocyte Differentiation

doi: 10.1002/jcp.25248

Figure Lengend Snippet: DUSP and inflammatory genes analyzed in this study

Article Snippet: For adipocytes, these stimuli include insulin and the synthetic glucocorticoid dexamethasone ( Kusari et al., 1997 ; Kassel et al., 2001 ). table ft1 table-wrap mode="anchored" t5 caption a7 Symbol Name/alias Accession ABI number C T Dual specificity phosphatases GP MKB NLS NES EJP Dusp1 MKP-1,hVH1 I ● ● NM_013642 Mm00457274_g1 24 Dusp2 PAC-1 I ● ● NM_010090 Mm00839675_g1 30 Dusp4 MKP-2, hVH2 I ● ● NM_176933 Mm00723761_m1 25 Dusp5 hVH3 I ● ● NM_001085390 Mm01266104_m1 27 Dusp6 MKP-3, rVH6 II ● ● E NM_026268 Mm00650255_g1 24 Dusp7 MKP-X II ● ● E NM_153459 Mm00463228_m1 27 Dusp9 MKP-4 II ● ● E NM_029352 Mm00512646_m1 27 Dusp8 M3/6, hVH5 III ● ● ● J/P NM_008748 Mm00456230_m1 27 Dusp10 MKP-5 III ● J/P NM_022019 Mm00517678_m1 24 Dusp16 MKP-7, MKP-M III ● ● ● J/P NM_130447 Mm00459935_m1 25 Inflammatory genes IL-6 Interleukin-6 NM_031168 Mm99999064_m1 32 TNFα Tumor necrosis factor-alpha NM_013693 Mm99999068_m1 28 Reference gene 18S 18 Ribosomal RNA X03205 4342930E 9 Open in a separate window DUSP group (GP), MAPK binding domain (MKB), nuclear localization sequence (NLS), nuclear export sequence (NES), ERK (E), JNK (J), p38 (P), threshold cycle (C T ) measured in lean adipose tissue.

Techniques:

Journal: Aging (Albany NY)

Article Title: Comprehensive analysis of scRNA-seq and bulk RNA-seq reveal the characteristics of disulfidptosis and a prognostic signature in BLCA

doi: 10.18632/aging.205686

Figure Lengend Snippet: Overexpression of DUSP2 inhibited the proliferation, migration, and invasion of BLCA cells. ( A , B ) Differential analysis and survival analysis of DUSP2. ( C ) The mRNA expression of DUSP2 in BLCA cells and normal bladder cells. ( D , E ) The overexpression efficiency of DUSP2 was confirmed by qRT–PCR and western blotting. ( F , G ) CCK-8 and EdU assay were conducted to evaluate the proliferation ability. ( H ) Wound healing assay for the migration ability. ( I ) Transwell assay for the invasion ability. * P < 0.05, ** P < 0.01.

Article Snippet: The membrane was blocked with 5% skim milk and then incubated with primary antibodies against SLCO1B3 (Cat No. 66381-1-Ig, 1:4000), DUSP2 (Cat No: 27327-1-AP, 1:1000) and GAPDH (Cat No. 60004-1-Ig, 1:20000) from Proteintech Company.

Techniques: Over Expression, Migration, Expressing, Quantitative RT-PCR, Western Blot, CCK-8 Assay, EdU Assay, Wound Healing Assay, Transwell Assay

Journal: Nature Communications

Article Title: Small-molecule-induced ERBB4 activation to treat heart failure

doi: 10.1038/s41467-024-54908-5

Figure Lengend Snippet: a Volcano plot showing differential gene expression (two-tailed DESeq2’s Wald test, P adj <0.05) of HCFs in response to EF-1 ( n = 3 biological replicates). The horizontal dashed line indicates -Log10 ( P adj <0.05). b Heatmap showing log2 fold change estimates for top DEGs in EF-1-treated HCFs relative to the control group. c Venn diagram of overlapping DEGs between the NRG1 and EF-1 group. d Heatmap showing log2 fold change estimates for top DEGs in EF-1- or NRG1-treated HCFs relative to the control group. e GSEA of HCFs with EF - 1 or NRG1 for gene signatures of TGF-β, PI3K/Akt and MAPK pathway-regulated genes. P -values were adjusted via the Benjamini–Hochberg procedure. f – h RT-qPCR on signaling pathway genes in HCFs; normalized FC compared to vehicle ( n = 4 biological replicates for every value in each group): f ID2 and BMPR1B , genes involved in TGFβ signaling, g CACNA2D4 and DUSP2 , genes involved in MAPK/ERK signaling and h NR4A1 and SGK1 , genes involved in PI3k-Akt signaling. All data are represented as mean ± SD, one-way ANOVA with Tukey’s multiple comparisons test. Source data are provided as a Source Data file. Akt protein kinase B, ANOVA analysis of variance, BMPR1B bone morphogenetic protein receptor type 1B, CACNA2D4 calcium voltage-gated channel auxiliary subunit alpha-2 delta-4, DEG differentially expressed gene, DUSP2 dual specificity phosphatase 2, ERK extracellular signal-regulated kinase, FC fold change, GSEA gene set enrichment analysis, HCF human cardiac fibroblast, ID2 Inhibitor of DNA Binding 2, MAPK mitogen-activated protein kinase, NES normalized enrichment score, NRG1 neuregulin-1, NR4A1 nuclear receptor subfamily 4 group A member 1, PI3K phosphatidylinositol 3-kinase, RT-qPCR real-time quantitative polymerase chain reaction, SGK1 serum/glucocorticoid-regulated kinase 1, TGF-β transforming growth factor-β.

Article Snippet: The following TaqMan primers were used (Thermo Fisher Scientific): GAPDH (Hs02758991_g1, Mm99999915_g1 and Rn01775763_g1), PGK1 (Hs99999906_m1), ID2 (Hs04187239_m1), BMPR1B (Hs01010965_m1), CACNA2D4 (Hs00297782_m1), DUSP2 (Hs00358879_m1), NR4A1 (Hs00374226_m1), SGK1 (Hs00178612_m1), COL1A1 (Mm00801666_g1), COL3A1 (Hs00943809_m1 and Mm00802305_g1), ERBB4 (Hs00955525_m1 and Rn00572447_m1), ACTB (Mm02619580_g1) and ANP (Mm01255747_g1).

Techniques: Gene Expression, Two Tailed Test, Control, Quantitative RT-PCR, Binding Assay, Real-time Polymerase Chain Reaction

Journal: Journal of Extracellular Vesicles

Article Title: DUSP2 regulates extracellular vesicle-VEGF-C secretion and pancreatic cancer early dissemination

doi: 10.1080/20013078.2020.1746529

Figure Lengend Snippet: Inhibition of DUSP2 increases VEGF-C expression . (a) Representative pictures of DUSP2 immunostaining in pancreatic tumours. PanIN: pancreatic intraepithelial neoplasia, Ca: invasive carcinoma, arrowhead: non-tumour elements. (b) Representative pictures of DUSP2 immunostaining in KPC tumours. Arrows: infiltrating cancer cells; circles: carcinoma (Ca). (c) Representative immunohistochemical staining images show the expression of ERK1/2 phosphorylation in LSL - Trp53 R172 H (WT) pancreas and KPC tumours. (d) Representative Western blots show the expression of phosphorylated ERK (left), EV-VEGF-C (middle) in MIA PaCa-2 cells treated without (DMSO) or with ERK inhibitor, SCH 772984 (1 μM, SCH) for 24 h. EVs were isolated by ultracentrifugation (Ultra) or ExoQuick-TC (ExoQ) exosome precipitation reagent. The right panel shows EV-VEGF-C in AsPC-1-Ctrl and AsPC-1-VEGF-C cells treated with DMSO or SCH 772984 (1 μM, SCH). EV in AsPC-1 was isolated by ExoQuick-TC. Annexin V and CD63 were used as markers of EVs in MIA PaCa-2 and AsPC-1 cells, respectively. (e) Representative image shows levels of DUSP2 in human pancreatic cancer cell lines PANC-1 and MIA PaCa-2 (left) and levels of DUSP2, total and phospho-ERK in control and DUSP2-KD PANC-1 cells (right). DU#1 and DU#2 indicate two stable clones of PANC-1 cells with DUSP2 knockdown. β-actin is a loading control. (f) VEGF-A and VEGF-C were measured in control and DUSP2-KD PANC-1 cells by RT-qPCR. Data represent mean and SEM of three experiments using different batches of cells (left). Representative image and the quantitative result (right) show the increase of secreted VEGF-C in DUSP2-KD PANC-1 cells. Ponceau S staining was employed to examine the equal loading of proteins. (g) RT-PCR and Western blotting for the detection of VEGF-C mRNA and secreted protein in control and DUSP2-KD PANC-1 cells treated with U0126 (10 μM). (h) Representative Western image shows levels of DUSP2 and VEGF-C in cells with or without transient expression of DUSP2 in MIA PaCa-2 cells. Secreted VEGF-C was quantified in control and DUSP2 transfected MIA PaCa-2 cells (right). (i) Inverse expression of DUSP2 and VEGF-C in mouse tissues. Various tissues from male BALB/c mice were collected and homogenized. Western blotting was performed to measure the expression of DUSP2 and VEGF-C. * P < 0.05; ** P < 0.01; *** P < 0.001.

Article Snippet: Five arrays were used for immunohistochemistry staining of DUSP2 (Genetex).

Techniques: Inhibition, Expressing, Immunostaining, Immunohistochemical staining, Staining, Phospho-proteomics, Western Blot, Isolation, Control, Clone Assay, Knockdown, Quantitative RT-PCR, Reverse Transcription Polymerase Chain Reaction, Transfection

Journal: Journal of Extracellular Vesicles

Article Title: DUSP2 regulates extracellular vesicle-VEGF-C secretion and pancreatic cancer early dissemination

doi: 10.1080/20013078.2020.1746529

Figure Lengend Snippet: DUSP2 knockdown promotes lymphangiogenesis and lymphovascular invasion in the orthotopic pancreatic cancer mouse model . (a) Conditioned media from DUSP2-KD PANC-1 cells enhanced the proliferation of LECs. Conditioned media from control and DUSP2-KD PANC-1 cells were used to treat LECs with or without the addition of VEGFR2/R3 inhibitor, Lenvatinib (10 nM). Data represent mean and SEM of three independent experiments using conditioned media collected from different batches of cells. (b) Representative pictures (left) and quantitative result (right, n = 3) show conditioned media from DUSP2-KD PANC-1 cells promoted migration of LECs. * P < 0.05; *** P < 0.001. (c) Representative picture of tumours developed in the pancreas of mice when injected with PANC-1 control and DUSP2-KD cells. (d) Representative images show the increase of lymphatic vessels in DUSP2-KD orthotopic injected tumours compared with that in control tumours. Lymphatic marker Lyve-1 was used to identify lymphatic vessels. CD31 was used to identify blood vessels. Original magnification, ×200. (e) Example of lymphovascular invasion and lymph node metastasis by H&E stain. No tumour cells were present in the lymphatic/blood vessels in mice injected with control PANC-1 cells while tumour emboli were seen in mice injected with DUSP2-KD PANC-1 cells. Asterisk represents tumour cells. Fisher’s exact test (two sided) indicates a significant increase in the number of mice with lymphovascular invasion (LVI) and nodal metastasis (LNM) if they are bearing DUSP2-KD tumours ( P = 0.01). Tumours were sliced as serial sections and H&E-stained histologic sections were scored in a blinded manner by a pathologist (bottom right). (f) Schematic drawings illustrate the strategy of generating conditional knockout of Dusp2 in the pancreas of mice (top). Representative image of genotyping result by PCR (middle). Representative immunohistochemical staining images show expression of Lyve-1 in the pancreas of 4 months old wild type (WT) and Dusp2 knockout (Dusp2 −/- ) mice (bottom). Original magnification, ×200. (g) Representative immunohistochemical staining images show expression of phosphorylated ERK, Lyve-1 and CD31 in serial sections in the pancreas of 7 months old wild type (WT) and LSL-Kras G12D ; LSL-Dusp2; Pdx1-cre (KDC) mice. Original magnification, ×200. (h) The expression of VEGF-C is increased in EV isolated from serum in KDC mice. Western blotting was performed for the detection of VEGF-C and CD63. Ponceau S staining was used as control for equal amount of protein loading.

Article Snippet: Five arrays were used for immunohistochemistry staining of DUSP2 (Genetex).

Techniques: Knockdown, Control, Migration, Injection, Marker, Staining, Knock-Out, Immunohistochemical staining, Expressing, Isolation, Western Blot

Journal: Journal of Extracellular Vesicles

Article Title: DUSP2 regulates extracellular vesicle-VEGF-C secretion and pancreatic cancer early dissemination

doi: 10.1080/20013078.2020.1746529

Figure Lengend Snippet: Knockdown of DUSP2 mediates autocrine function in pancreatic cancer cells via VEGF-C signalling . (a) Representative image shows the morphology of control and DUSP2 knockdown in PANC-1 cells. (b) Representative image (left) and the quantitative result (right, n = 3) show the migration ability in DUSP2-KD PANC-1 cells. Control (ctrl) and DUSP2-KD (DU#1 and DU#2) PANC-1cells were seeded in the 24-well plate to confluent and a straight scratch was made by pipette tips. Images were recorded and analysed after 24 h. (c) Representative image (left) and the quantitative result (right, n = 3) show cell invasion ability in control and DUSP2-KD PANC-1 cells. (d) Expression of DUSP2-GFP in MIA PaCa-2 cells inhibited cell migration through transwell. MIA PaCa-2 cells were transfected with GFP or DUSP2-GFP, equal numbers of cells were plated on top of transwell. Data represent mean and SEM from two independent experiments (performed in triplicate) using different batches of cells. (e) Representative images (left) and the quantitative result (right, n = 3) show increased invasion ability in DUSP2-KD PANC-1 cells was suppressed when treated with VEGFR2/R3 inhibitor, Lenvatinib (10 nM). * P < 0.05 compared to control, # P < 0.05 compared to DUSP2-KD. (f) Representative images (left panels) and quantitative result (right, n = 3) show knockdown of VEGF-C abolished loss-of-DUSP2-mediated increased invasion ability. VEGF-C was transient knocked down in control and DUSP2-KD PANC-1 cells. Cell invasion ability was measured in matrigel-coated transwell. * P < 0.05 compared to control, # P < 0.05 compared to DUSP2-KD. (g) Schematic diagram (top) and quantitative result (bottom, n = 3) show increased transendothelial migration assay in control and DUSP2-KD PANC-1 cells were suppressed when treated with VEGFR2/R3 inhibitor. Endothelial cells were seeded to a matrigel-coated transwell. After the endothelial layer was formed, PANC-1 control and DUSP2-KD cells were added to the chamber and transendothelial migration ability was measured after 16 h. * P < 0.05 compared to control, # P < 0.05 compared to DUSP2-KD. * P < 0.05; ** P < 0.01.

Article Snippet: Five arrays were used for immunohistochemistry staining of DUSP2 (Genetex).

Techniques: Knockdown, Control, Migration, Transferring, Expressing, Transfection

Journal: Journal of Extracellular Vesicles

Article Title: DUSP2 regulates extracellular vesicle-VEGF-C secretion and pancreatic cancer early dissemination

doi: 10.1080/20013078.2020.1746529

Figure Lengend Snippet: DUSP2 regulates VEGF-C expression mainly via post-translational modification . (a) Representative Western blots show expression of VEGF-C in conditioned media of control and DUSP2-KD PANC-1 cells at different time points. Angiogenin (ANG) was used as a loading control in conditioned medium. (b) AsPC1-VEGF-C cells were treated with cycloheximide (CHX) and BFA to block protein synthesis and protein secretion. The size of prepro-VEGF-C, pro-VEGF-C and processed VEGF-C was detected as indicated. (c) AsPC1-VEGF-C cells were transiently transfected with GFP or DUSP2-GFP plasmids and levels of DUSP2, VEGF-C in whole cell lysate (WCL) and conditioned medium (CM) were detected. (d) Proprotein convertase activity in control and DUSP2-KD PANC-1 cells. Cell lysates of control and DUSP2-KD cells were incubated with two different concentrations of fluorogenic proprotein convertase substrate. Fluorescent was measured in a kinetic manner with Ex: 360–380 nm, Em: 440–460 nm. Representative quantification (of three independent experiments) is shown. (e) Proprotein convertase activity was measured in control and DUSP2-KD PANC-1 cells treated with proprotein convertase inhibitor for 24 h. (f) Representative images (left) and the quantitative result ( n = 3, right) show loss-of-DUSP2-enhanced VEGF-C secretion was inhibited by treatment with proprotein convertase inhibitor. Control and DUSP2-KD PANC-1 cells were treated with proprotein convertase inhibitor (20 μM) in serum-free RPMI medium. After 24 h, serum-free conditioned media were collected and VEGF-C expression was measured. ** P < 0.01 compared to control, # P < 0.05 compared to DUSP2-KD. (g) Control and DUSP2-KD cells were pre-treated with proprotein convertase inhibitor and plated for invasion ability. Recombinant VEGF-C was treated in the upper chamber of transwell. * P < 0.05.

Article Snippet: Five arrays were used for immunohistochemistry staining of DUSP2 (Genetex).

Techniques: Expressing, Modification, Western Blot, Control, Blocking Assay, Transfection, Activity Assay, Incubation, Recombinant

Journal: Journal of Extracellular Vesicles

Article Title: DUSP2 regulates extracellular vesicle-VEGF-C secretion and pancreatic cancer early dissemination

doi: 10.1080/20013078.2020.1746529

Figure Lengend Snippet: DUSP2 regulates the secretion of EV-VEGF-C in pancreatic cancer cells . (a) Representative (upper) and quantification (bottom) of VEGF-C and HSP70 expression by Western blotting in EV (isolated by ExoQuick-TC) from control and DUSP2-KD PANC-1 cells. (b) Representative Western blots show VEGF-C expression in WCL, EV and CM in DUSP2-KD PANC-1 cells (left). Representative Western blots show VEGF-C expression in EV isolated from DUSP2-KD PANC-1 cells treated with DMSO (control) and SCH 772984 (1uM) for 24 h (right). CD63 and HSP70 were detected as EV markers. ALB was detected to demonstrate the purity of EV. Equal amount of protein (20 ug) was loaded. EV was isolated by ExoQuick-TC. (c) Images of control and DUSP2-KD PANC-1 cells transfected with VEGF-C-SNAP tag for 24 h. Cells were treated with proprotein convertase inhibitor in serum-free medium for another 24 h after transfection. After labelling by the fluorescent substrate for SNAP, cells were fixed and imaged. (d) Images of control and DUSP2-KD PANC-1 cells taken by the transmission electron microscope. Red arrows indicate positive staining by 10 nm gold labelled anti-VEGF-C antibody. (e) Nanoparticle Tracking Analysis (NTA) was performed to detect secreted particles from control and DUSP2-KD cells. Serum-free conditioned medium was collected and centrifuged to remove debris and were sent for NTA. The X-axis represents the size of particles and the Y-axis represents the number of particles secreted per cell. DUSP2-KD cells have increased numbers of EV ranging from 85 to 155 nm (middle panel). EV secreted from DUSP2-KD cells was diminished if treated with GW4869 (20 μM) (right panel). (f) Inverted light sheet microscope (Luxengo) was used to track fast-moving particles in control and DUSP2-KD cells. Cells were labelled with PKH67 and plated into the cell holder for the tracking of PKH67 positive particles within the cells. 3D tracking of PKH67 particles in control and DUSP2-KD cells analysed by Imaris software (left). Particles in DUSP2-KD cells have increased speed (upper right) and track length (bottom right). Experiments have been performed two times and represented data are shown. (g) DUSP2-KD cells have an increased rate of EV-VEGF-C secretion. VE-Snaptag was stably expressed in control and DUSP2-KD cells. Cells were treated with proprotein convertase inhibitor (20 uM) in serum-free RPMI. EV was isolated from the medium at a different time point. Western blotting was performed to detect unprocessed VEGF-C (VE-Snap) in EV (upper). Expression of EV-VEGF-C in control and DUSP2-KD cells by fold change analysis over 2 h (lower). (h) Schematic of experimental design to investigate the function of EV from DUSP2-KD PANC-1 cells (left). Representative immunohistochemistry images show the increase of lymphatic vessels (Lyve-1) in PANC-1 tumours treated with EV isolated from DUSP2-KD cells.

Article Snippet: Five arrays were used for immunohistochemistry staining of DUSP2 (Genetex).

Techniques: Expressing, Western Blot, Isolation, Control, Transfection, Transmission Assay, Microscopy, Staining, Software, Stable Transfection, Immunohistochemistry

Journal: Journal of Extracellular Vesicles

Article Title: DUSP2 regulates extracellular vesicle-VEGF-C secretion and pancreatic cancer early dissemination

doi: 10.1080/20013078.2020.1746529

Figure Lengend Snippet: A proposed model shows the role of DUSP2-VEGF-C axis in promoting pancreatic cancer progression . Downregulation of DUSP2 in pancreatic cancer cells leads to ERK phosphorylation which enhances proprotein convertase activity. Therefore, the production of a functional form of VEGF-C is increased. On the other hand, the amount and moving ability of EV are increased in DUSP2 knockdown cells, which enhance the secretion of functional VEGF-C to the tumour microenvironment. Increased EV-VEGF-C can promote lymphangiogenesis and enhances pancreatic cancer cell invasive ability, leading to lymphovascular invasion.

Article Snippet: Five arrays were used for immunohistochemistry staining of DUSP2 (Genetex).

Techniques: Phospho-proteomics, Activity Assay, Functional Assay, Knockdown

Journal: Open Life Sciences

Article Title: DUSP2 inhibits the progression of lupus nephritis in mice by regulating the STAT3 pathway

doi: 10.1515/biol-2022-0649

Figure Lengend Snippet: Low expression of DUSP2 in LN. (a) Expression of DUSP2 in normal and LN kidney tissues obtained from GSE112943 expression profile. (b) The mRNA expression levels of DUSP2 in normal and LN kidney tissues. (c) Protein expression levels of DUSP2 in normal and LN renal tissues. *** P < 0.001 vs control.

Article Snippet: The membrane was blocked by 5% skim milk and incubated with DUSP2 (Solarbio, K009050P, 1:1,000, China), p-STAT3 (Beyotime, AF5941, 1:1,000, China), STAT3 (Beyotime, AF1492, 1:1,000), COX2 (GeneTex, GTX60935, 1:1,000, USA), and GAPDH (GeneTex, GTX100118, 1:5,000) antibodies overnight at 4°C in a refrigerator.

Techniques: Expressing, Control

Journal: Open Life Sciences

Article Title: DUSP2 inhibits the progression of lupus nephritis in mice by regulating the STAT3 pathway

doi: 10.1515/biol-2022-0649

Figure Lengend Snippet: DUSP2 ameliorates renal tissue lesions in mice with LN. (a) Expression levels of DUSP2 protein in kidney tissues of various groups of mice. (b) Changes in proteinuria levels of mice in each group from 12 to 20 weeks. (c) Serum urea nitrogen levels in all groups of mice. (d) Serum dsDNA levels in each group of mice. (e) Renal histopathology of mice in each group *** P < 0.001 vs vector.

Article Snippet: The membrane was blocked by 5% skim milk and incubated with DUSP2 (Solarbio, K009050P, 1:1,000, China), p-STAT3 (Beyotime, AF5941, 1:1,000, China), STAT3 (Beyotime, AF1492, 1:1,000), COX2 (GeneTex, GTX60935, 1:1,000, USA), and GAPDH (GeneTex, GTX100118, 1:5,000) antibodies overnight at 4°C in a refrigerator.

Techniques: Expressing, Histopathology, Plasmid Preparation

Journal: Open Life Sciences

Article Title: DUSP2 inhibits the progression of lupus nephritis in mice by regulating the STAT3 pathway

doi: 10.1515/biol-2022-0649

Figure Lengend Snippet: DUSP2 reduces kidney tissue inflammation in mice with LN. (a) Serum TNF-α, IL-6, IL-1β content of mice in each group. (b) Expression of TNF-α, IL-6, IL-1β mRNA in kidney tissue of mice in each group. *** P < 0.001 vs vector.

Article Snippet: The membrane was blocked by 5% skim milk and incubated with DUSP2 (Solarbio, K009050P, 1:1,000, China), p-STAT3 (Beyotime, AF5941, 1:1,000, China), STAT3 (Beyotime, AF1492, 1:1,000), COX2 (GeneTex, GTX60935, 1:1,000, USA), and GAPDH (GeneTex, GTX100118, 1:5,000) antibodies overnight at 4°C in a refrigerator.

Techniques: Expressing, Plasmid Preparation

Journal: Open Life Sciences

Article Title: DUSP2 inhibits the progression of lupus nephritis in mice by regulating the STAT3 pathway

doi: 10.1515/biol-2022-0649

Figure Lengend Snippet: DUSP2 inhibits STAT3 activation. Expression of p-STAT3 and COX2 protein in kidney tissue of mice in each group. *** P < 0.001 vs vector.

Article Snippet: The membrane was blocked by 5% skim milk and incubated with DUSP2 (Solarbio, K009050P, 1:1,000, China), p-STAT3 (Beyotime, AF5941, 1:1,000, China), STAT3 (Beyotime, AF1492, 1:1,000), COX2 (GeneTex, GTX60935, 1:1,000, USA), and GAPDH (GeneTex, GTX100118, 1:5,000) antibodies overnight at 4°C in a refrigerator.

Techniques: Activation Assay, Expressing, Plasmid Preparation