Product: Phospho-JNK1/2/3 (Thr183+Tyr185) Antibody
Catalog: AF3318
Description: Rabbit polyclonal antibody to Phospho-JNK1/2/3 (Thr183+Tyr185)
Application: WB IHC IF/ICC
Cited expt.: WB, IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
Mol.Wt.: 46,54kDa; 48kD,53kD(Calculated).
Uniprot: P45983 | P45984 | P53779
RRID: AB_2834737

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 100ul $280 In stock
 200ul $350 In stock

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Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:100-1:500, IF/ICC 1:100-1:500
*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
Prediction:
Pig(100%), Bovine(100%), Horse(100%), Sheep(100%), Rabbit(100%), Dog(100%), Chicken(100%), Xenopus(100%)
Clonality:
Polyclonal
Specificity:
Phospho-JNK1/2/3 (Thr183+Tyr185) Antibody detects endogenous levels of JNK1/2/3 only when phosphorylated at Threonine 183+Tyrosine 185.
RRID:
AB_2834737
Cite Format: Affinity Biosciences Cat# AF3318, RRID:AB_2834737.
Conjugate:
Unconjugated.
Purification:
The antibody is from purified rabbit serum by affinity purification via sequential chromatography on phospho-peptide and non-phospho-peptide affinity columns.
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

C Jun kinase 2; c Jun N terminal kinase 1; c Jun N terminal kinase 2; c Jun N terminal kinase 3; c-Jun N-terminal kinase 1; JNK 46; JNK 55; JNK; JNK-46; JNK1; JNK1A2; JNK2; JNK21B1/2; JNK2A; JNK2ALPHA; JNK2B; JNK2BETA; JNK3 alpha protein kinase; JNK3; JNK3A; Jun kinase; JUN N terminal kinase; MAP kinase 10; MAP kinase 8; MAP kinase 9; MAP kinase p49 3F12; MAPK 10; MAPK 8; MAPK 9; MAPK10; mapk8; MAPK9; Mitogen activated protein kinase 10; Mitogen activated protein kinase 8; Mitogen activated protein kinase 8 isoform JNK1 alpha1; Mitogen activated protein kinase 8 isoform JNK1 beta2; Mitogen activated protein kinase 9; Mitogen-activated protein kinase 8; MK08_HUMAN; p493F12; p54a; p54aSAPK; p54bSAPK; PRKM10; PRKM8; PRKM9; SAPK; SAPK(beta); SAPK1; SAPK1a; SAPK1b; SAPK1c; Stress activated protein kinase 1; Stress activated protein kinase 1a; Stress activated protein kinase 1b; Stress activated protein kinase 1c; Stress activated protein kinase beta; Stress activated protein kinase JNK1; Stress activated protein kinase JNK2; Stress activated protein kinase JNK3; Stress-activated protein kinase 1c; Stress-activated protein kinase JNK1; c Jun kinase 2; C Jun N terminal kinase 2; c-Jun N-terminal kinase 2; JNK 55; JNK-55; JNK2 alpha; JNK2; JNK2 beta; JNK2A; JNK2alpha; JNK2B; JNK2BETA; Jun kinase; MAP kinase 9; MAPK 9; Mapk9; Mitogen activated protein kinase 9; Mitogen-activated protein kinase 9; MK09_HUMAN; P54a; p54aSAPK; PRKM9; Protein kinase, mitogen-activated, 9; SAPK alpha; SAPK; SAPK1a; Stress activated protein kinase 1a; Stress-activated protein kinase JNK2; c Jun kinase 3; c-Jun N-terminal kinase 3; cJun N terminal kinase 3; FLJ12099; FLJ33785; JNK3 alpha protein kinase; JNK3; JNK3A; MAP kinase 10; MAP kinase; MAP kinase p49 3F12; MAPK 10; Mapk10; MGC50974; mitogen activated protein kinase 10; Mitogen-activated protein kinase 10; MK10_HUMAN; p493F12; p54bSAPK; PRKM10; protein kinase mitogen activated 10; SAPK1b; Stress activated protein kinase 1b; stress activated protein kinase beta; Stress activated protein kinase JNK3; Stress-activated protein kinase JNK3;

Immunogens

Immunogen:

A synthesized peptide derived from human JNK1/2/3 around the phosphorylation site of Thr183+Tyr185.

Uniprot:
Gene(ID):
Expression:
P53779 MK10_HUMAN:

Specific to a subset of neurons in the nervous system. Present in the hippocampus and areas, cerebellum, striatum, brain stem, and weakly in the spinal cord. Very weak expression in testis and kidney.

Description:
JNK3 a protein kinase of the MAPK family that is potently activated by a variety of environmental stress and pro-inflammatory cytokines. Brain-selective JNK isoform.
Sequence:
MSRSKRDNNFYSVEIGDSTFTVLKRYQNLKPIGSGAQGIVCAAYDAILERNVAIKKLSRPFQNQTHAKRAYRELVLMKCVNHKNIIGLLNVFTPQKSLEEFQDVYIVMELMDANLCQVIQMELDHERMSYLLYQMLCGIKHLHSAGIIHRDLKPSNIVVKSDCTLKILDFGLARTAGTSFMMTPYVVTRYYRAPEVILGMGYKENVDLWSVGCIMGEMVCHKILFPGRDYIDQWNKVIEQLGTPCPEFMKKLQPTVRTYVENRPKYAGYSFEKLFPDVLFPADSEHNKLKASQARDLLSKMLVIDASKRISVDEALQHPYINVWYDPSEAEAPPPKIPDKQLDEREHTIEEWKELIYKEVMDLEERTKNGVIRGQPSPLGAAVINGSQHPSSSSSVNDVSSMSTDPTLASDTDSSLEAAAGPLGCCR

MSDSKCDSQFYSVQVADSTFTVLKRYQQLKPIGSGAQGIVCAAFDTVLGINVAVKKLSRPFQNQTHAKRAYRELVLLKCVNHKNIISLLNVFTPQKTLEEFQDVYLVMELMDANLCQVIHMELDHERMSYLLYQMLCGIKHLHSAGIIHRDLKPSNIVVKSDCTLKILDFGLARTACTNFMMTPYVVTRYYRAPEVILGMGYKENVDIWSVGCIMGELVKGCVIFQGTDHIDQWNKVIEQLGTPSAEFMKKLQPTVRNYVENRPKYPGIKFEELFPDWIFPSESERDKIKTSQARDLLSKMLVIDPDKRISVDEALRHPYITVWYDPAEAEAPPPQIYDAQLEEREHAIEEWKELIYKEVMDWEERSKNGVVKDQPSDAAVSSNATPSQSSSINDISSMSTEQTLASDTDSSLDASTGPLEGCR

MSLHFLYYCSEPTLDVKIAFCQGFDKQVDVSYIAKHYNMSKSKVDNQFYSVEVGDSTFTVLKRYQNLKPIGSGAQGIVCAAYDAVLDRNVAIKKLSRPFQNQTHAKRAYRELVLMKCVNHKNIISLLNVFTPQKTLEEFQDVYLVMELMDANLCQVIQMELDHERMSYLLYQMLCGIKHLHSAGIIHRDLKPSNIVVKSDCTLKILDFGLARTAGTSFMMTPYVVTRYYRAPEVILGMGYKENVDIWSVGCIMGEMVRHKILFPGRDYIDQWNKVIEQLGTPCPEFMKKLQPTVRNYVENRPKYAGLTFPKLFPDSLFPADSEHNKLKASQARDLLSKMLVIDPAKRISVDDALQHPYINVWYDPAEVEAPPPQIYDKQLDEREHTIEEWKELIYKEVMNSEEKTKNGVVKGQPSPSGAAVNSSESLPPSSSVNDISSMSTDQTLASDTDSSLEASAGPLGCCR

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
Xenopus
100
Chicken
100
Rabbit
100
Zebrafish
79
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

Research Backgrounds

Function:

Serine/threonine-protein kinase involved in various processes such as cell proliferation, differentiation, migration, transformation and programmed cell death. Extracellular stimuli such as proinflammatory cytokines or physical stress stimulate the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway. In this cascade, two dual specificity kinases MAP2K4/MKK4 and MAP2K7/MKK7 phosphorylate and activate MAPK8/JNK1. In turn, MAPK8/JNK1 phosphorylates a number of transcription factors, primarily components of AP-1 such as JUN, JDP2 and ATF2 and thus regulates AP-1 transcriptional activity. Phosphorylates the replication licensing factor CDT1, inhibiting the interaction between CDT1 and the histone H4 acetylase HBO1 to replication origins. Loss of this interaction abrogates the acetylation required for replication initiation. Promotes stressed cell apoptosis by phosphorylating key regulatory factors including p53/TP53 and Yes-associates protein YAP1. In T-cells, MAPK8 and MAPK9 are required for polarized differentiation of T-helper cells into Th1 cells. Contributes to the survival of erythroid cells by phosphorylating the antagonist of cell death BAD upon EPO stimulation. Mediates starvation-induced BCL2 phosphorylation, BCL2 dissociation from BECN1, and thus activation of autophagy. Phosphorylates STMN2 and hence regulates microtubule dynamics, controlling neurite elongation in cortical neurons. In the developing brain, through its cytoplasmic activity on STMN2, negatively regulates the rate of exit from multipolar stage and of radial migration from the ventricular zone. Phosphorylates several other substrates including heat shock factor protein 4 (HSF4), the deacetylase SIRT1, ELK1, or the E3 ligase ITCH. Phosphorylates the CLOCK-ARNTL/BMAL1 heterodimer and plays a role in the regulation of the circadian clock. Phosphorylates the heat shock transcription factor HSF1, suppressing HSF1-induced transcriptional activity. Phosphorylates POU5F1, which results in the inhibition of POU5F1's transcriptional activity and enhances its proteosomal degradation (By similarity). Phosphorylates JUND and this phosphorylation is inhibited in the presence of MEN1 (By similarity). In neurons, phosphorylates SYT4 which captures neuronal dense core vesicles at synapses (By similarity).

JNK1 isoforms display different binding patterns: beta-1 preferentially binds to c-Jun, whereas alpha-1, alpha-2, and beta-2 have a similar low level of binding to both c-Jun or ATF2. However, there is no correlation between binding and phosphorylation, which is achieved at about the same efficiency by all isoforms.

PTMs:

Dually phosphorylated on Thr-183 and Tyr-185 by MAP2K7 and MAP2K4, which activates the enzyme. Phosphorylated by TAOK2. May be phosphorylated at Thr-183 and Tyr-185 by MAP3K1/MEKK1. Phosphorylated form is more concentrated at synapses than none-phosphorylated (By similarity).

Subcellular Location:

Cytoplasm. Nucleus. Cell junction>Synapse.
Note: In the cortical neurons, predominantly cytoplasmic and associated with the Golgi apparatus and endosomal fraction. Increased neuronal activity increases phosphorylated form at synapses (By similarity). Colocalizes with POU5F1 in the nucleus.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Family&Domains:

The TXY motif contains the threonine and tyrosine residues whose phosphorylation activates the MAP kinases.

Belongs to the protein kinase superfamily. CMGC Ser/Thr protein kinase family. MAP kinase subfamily.

Function:

Serine/threonine-protein kinase involved in various processes such as cell proliferation, differentiation, migration, transformation and programmed cell death. Extracellular stimuli such as proinflammatory cytokines or physical stress stimulate the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway. In this cascade, two dual specificity kinases MAP2K4/MKK4 and MAP2K7/MKK7 phosphorylate and activate MAPK9/JNK2. In turn, MAPK9/JNK2 phosphorylates a number of transcription factors, primarily components of AP-1 such as JUN and ATF2 and thus regulates AP-1 transcriptional activity. In response to oxidative or ribotoxic stresses, inhibits rRNA synthesis by phosphorylating and inactivating the RNA polymerase 1-specific transcription initiation factor RRN3. Promotes stressed cell apoptosis by phosphorylating key regulatory factors including TP53 and YAP1. In T-cells, MAPK8 and MAPK9 are required for polarized differentiation of T-helper cells into Th1 cells. Upon T-cell receptor (TCR) stimulation, is activated by CARMA1, BCL10, MAP2K7 and MAP3K7/TAK1 to regulate JUN protein levels. Plays an important role in the osmotic stress-induced epithelial tight-junctions disruption. When activated, promotes beta-catenin/CTNNB1 degradation and inhibits the canonical Wnt signaling pathway. Participates also in neurite growth in spiral ganglion neurons. Phosphorylates the CLOCK-ARNTL/BMAL1 heterodimer and plays a role in the regulation of the circadian clock. Phosphorylates POU5F1, which results in the inhibition of POU5F1's transcriptional activity and enhances its proteosomal degradation (By similarity).

MAPK9 isoforms display different binding patterns: alpha-1 and alpha-2 preferentially bind to JUN, whereas beta-1 and beta-2 bind to ATF2. However, there is no correlation between binding and phosphorylation, which is achieved at about the same efficiency by all isoforms. JUNB is not a substrate for JNK2 alpha-2, and JUND binds only weakly to it.

PTMs:

Dually phosphorylated on Thr-183 and Tyr-185 by MAP2K7 and MAP2K4, which activates the enzyme. Autophosphorylated in vitro.

Subcellular Location:

Cytoplasm. Nucleus.
Note: Colocalizes with POU5F1 in the nucleus.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Family&Domains:

The TXY motif contains the threonine and tyrosine residues whose phosphorylation activates the MAP kinases.

Belongs to the protein kinase superfamily. CMGC Ser/Thr protein kinase family. MAP kinase subfamily.

Function:

Serine/threonine-protein kinase involved in various processes such as neuronal proliferation, differentiation, migration and programmed cell death. Extracellular stimuli such as proinflammatory cytokines or physical stress stimulate the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway. In this cascade, two dual specificity kinases MAP2K4/MKK4 and MAP2K7/MKK7 phosphorylate and activate MAPK10/JNK3. In turn, MAPK10/JNK3 phosphorylates a number of transcription factors, primarily components of AP-1 such as JUN and ATF2 and thus regulates AP-1 transcriptional activity. Plays regulatory roles in the signaling pathways during neuronal apoptosis. Phosphorylates the neuronal microtubule regulator STMN2. Acts in the regulation of the amyloid-beta precursor protein/APP signaling during neuronal differentiation by phosphorylating APP. Participates also in neurite growth in spiral ganglion neurons. Phosphorylates the CLOCK-ARNTL/BMAL1 heterodimer and plays a role in the photic regulation of the circadian clock. Phosphorylates JUND and this phosphorylation is inhibited in the presence of MEN1.

PTMs:

Dually phosphorylated on Thr-221 and Tyr-223 by MAP2K4 and MAP2K7, which activates the enzyme. MAP2K7 shows a strong preference for Thr-221 while MAP2K4 phosphorylates Tyr-223 preferentially. Weakly autophosphorylated on threonine and tyrosine residues in vitro.

Palmitoylation regulates subcellular location and axonal development.

Subcellular Location:

Cytoplasm. Membrane>Lipid-anchor. Nucleus. Mitochondrion.
Note: Palmitoylation regulates MAPK10 trafficking to cytoskeleton. Recruited to the mitochondria in the presence of SARM1 (By similarity).

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Specific to a subset of neurons in the nervous system. Present in the hippocampus and areas, cerebellum, striatum, brain stem, and weakly in the spinal cord. Very weak expression in testis and kidney.

Family&Domains:

The TXY motif contains the threonine and tyrosine residues whose phosphorylation activates the MAP kinases.

Belongs to the protein kinase superfamily. CMGC Ser/Thr protein kinase family. MAP kinase subfamily.

Research Fields

· Cellular Processes > Transport and catabolism > Autophagy - animal.   (View pathway)

· Cellular Processes > Cell growth and death > Apoptosis.   (View pathway)

· Cellular Processes > Cell growth and death > Apoptosis - multiple species.   (View pathway)

· Cellular Processes > Cell growth and death > Necroptosis.   (View pathway)

· Cellular Processes > Cellular community - eukaryotes > Focal adhesion.   (View pathway)

· Cellular Processes > Cellular community - eukaryotes > Tight junction.   (View pathway)

· Environmental Information Processing > Signal transduction > MAPK signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > ErbB signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Ras signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > cAMP signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > FoxO signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Sphingolipid signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Wnt signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > TNF signaling pathway.   (View pathway)

· Genetic Information Processing > Folding, sorting and degradation > Protein processing in endoplasmic reticulum.   (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > Endocrine resistance.

· Human Diseases > Endocrine and metabolic diseases > Type II diabetes mellitus.

· Human Diseases > Endocrine and metabolic diseases > Insulin resistance.

· Human Diseases > Endocrine and metabolic diseases > Non-alcoholic fatty liver disease (NAFLD).

· Human Diseases > Infectious diseases: Bacterial > Epithelial cell signaling in Helicobacter pylori infection.

· Human Diseases > Infectious diseases: Bacterial > Shigellosis.

· Human Diseases > Infectious diseases: Bacterial > Salmonella infection.

· Human Diseases > Infectious diseases: Bacterial > Pertussis.

· Human Diseases > Infectious diseases: Parasitic > Chagas disease (American trypanosomiasis).

· Human Diseases > Infectious diseases: Parasitic > Toxoplasmosis.

· Human Diseases > Infectious diseases: Bacterial > Tuberculosis.

· Human Diseases > Infectious diseases: Viral > Hepatitis C.

· Human Diseases > Infectious diseases: Viral > Hepatitis B.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Human Diseases > Infectious diseases: Viral > HTLV-I infection.

· Human Diseases > Infectious diseases: Viral > Herpes simplex infection.

· Human Diseases > Infectious diseases: Viral > Epstein-Barr virus infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Colorectal cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Pancreatic cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Choline metabolism in cancer.   (View pathway)

· Organismal Systems > Development > Osteoclast differentiation.   (View pathway)

· Organismal Systems > Immune system > Toll-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > NOD-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > RIG-I-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > IL-17 signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Th1 and Th2 cell differentiation.   (View pathway)

· Organismal Systems > Immune system > Th17 cell differentiation.   (View pathway)

· Organismal Systems > Immune system > T cell receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Fc epsilon RI signaling pathway.   (View pathway)

· Organismal Systems > Nervous system > Neurotrophin signaling pathway.   (View pathway)

· Organismal Systems > Nervous system > Retrograde endocannabinoid signaling.   (View pathway)

· Organismal Systems > Nervous system > Dopaminergic synapse.

· Organismal Systems > Sensory system > Inflammatory mediator regulation of TRP channels.   (View pathway)

· Organismal Systems > Endocrine system > Insulin signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Progesterone-mediated oocyte maturation.

· Organismal Systems > Endocrine system > Prolactin signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Adipocytokine signaling pathway.

· Organismal Systems > Endocrine system > Relaxin signaling pathway.

References

1). SARS-CoV-2 envelope protein impairs airway epithelial barrier function and exacerbates airway inflammation via increased intracellular Cl- concentration. Signal transduction and targeted therapy, 2024 (PubMed: 38528022) [IF=40.8]

Application: WB    Species: Human    Sample:

Fig. 7 SARS-CoV-2 envelope (E) protein down-regulated tight junction proteins and triggered inflammation and intracellular Cl− accumulation in human primary cultured airway epithelial cells (hPAECs). a Representative immunoblots showing the expression level of ZO-1, occludin and claudin-4 in hPAECs stimulated with E protein (50 μg/ml) for 6 h. GAPDH served as a loading control. b Immunofluorescence images showing the expression of ZO-1 in hPAECs, in the absence or presence of E protein stimulation for 6 h. c Quantitative real-time PCR analyses showing the expression of pro-inflammatory cytokines in hPAECs stimulated with E protein (50 μg/ml) for 12 h (n = 3). d Representative immunoblots showing the expression of cystic fibrosis transmembrane conductance regulator (CFTR) and the phosphorylation level of JNK, serum/glucocorticoid regulated kinase 1 (SGK1) and IκB in hPAECs after stimulation with the E protein (50 μg/ml) for 12 h. GAPDH served as a loading control. e Immunofluorescence images showing the phosphorylation of JNK in hPAECs, in the absence or presence of E protein (50 μg/ml) stimulation. f Immunofluorescence images showing the phosphorylation of SGK1 in hPAECs, in the absence or presence of E protein (50 μg/ml) stimulation. g Quantitative real-time PCR analyses showing the expression of phosphodiesterase 4 (PDE4) in hPAECs stimulated with E protein (50 μg/ml) for the indicated different time points (n = 3). h Intracellular Cl− concentration ([Cl−]i) was measured in hPAECs stimulated with E protein (50 μg/ml) for 12 h (n = 25 cells for each group). Data are shown as means ± S.D. **P 

Application: IF/ICC    Species: Human    Sample: BEAS-2B cells

Fig. 7 SARS-CoV-2 envelope (E) protein down-regulated tight junction proteins and triggered inflammation and intracellular Cl− accumulation in human primary cultured airway epithelial cells (hPAECs). a Representative immunoblots showing the expression level of ZO-1, occludin and claudin-4 in hPAECs stimulated with E protein (50 μg/ml) for 6 h. GAPDH served as a loading control. b Immunofluorescence images showing the expression of ZO-1 in hPAECs, in the absence or presence of E protein stimulation for 6 h. c Quantitative real-time PCR analyses showing the expression of pro-inflammatory cytokines in hPAECs stimulated with E protein (50 μg/ml) for 12 h (n = 3). d Representative immunoblots showing the expression of cystic fibrosis transmembrane conductance regulator (CFTR) and the phosphorylation level of JNK, serum/glucocorticoid regulated kinase 1 (SGK1) and IκB in hPAECs after stimulation with the E protein (50 μg/ml) for 12 h. GAPDH served as a loading control. e Immunofluorescence images showing the phosphorylation of JNK in hPAECs, in the absence or presence of E protein (50 μg/ml) stimulation. f Immunofluorescence images showing the phosphorylation of SGK1 in hPAECs, in the absence or presence of E protein (50 μg/ml) stimulation. g Quantitative real-time PCR analyses showing the expression of phosphodiesterase 4 (PDE4) in hPAECs stimulated with E protein (50 μg/ml) for the indicated different time points (n = 3). h Intracellular Cl− concentration ([Cl−]i) was measured in hPAECs stimulated with E protein (50 μg/ml) for 12 h (n = 25 cells for each group). Data are shown as means ± S.D. **P 

2). Hepatoma cell-intrinsic TLR9 activation induces immune escape through PD-L1 upregulation in hepatocellular carcinoma. Theranostics, 2023 (PubMed: 32483468) [IF=12.4]

3). Mucin 17 inhibits the progression of human gastric cancer by limiting inflammatory responses through a MYH9-p53-RhoA regulatory feedback loop. JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH, 2019 (PubMed: 31262330) [IF=11.3]

Application: WB    Species: human    Sample: AGS cells

Fig. 5| MUC17 protects GC cells against inflammatory stimulation by regulating the p38 pathway. a MUC17 regulated the expression of pJNK,pERK, and pp38 MAPK in MUC17 knocked-down AGS cells (left) and truncated MUC17 overexpressed MKN45 cells (right).

4). The microRNA-211-5p/P2RX7/ERK/GPX4 axis regulates epilepsy-associated neuronal ferroptosis and oxidative stress. Journal of neuroinflammation, 2024 (PubMed: 38191407) [IF=9.3]

5). Elamipretide alleviates pyroptosis in traumatically injured spinal cord by inhibiting cPLA2-induced lysosomal membrane permeabilization. Journal of Neuroinflammation, 2023 (PubMed: 36609266) [IF=9.3]

6). LAGE3 promoted cell proliferation, migration, and invasion and inhibited cell apoptosis of hepatocellular carcinoma by facilitating the JNK and ERK signaling pathway. CELLULAR & MOLECULAR BIOLOGY LETTERS, 2021 (PubMed: 34837962) [IF=9.2]

Application: WB    Species: Human    Sample: Hep-3B cells

Fig. 6 LAGE3 aggravated HCC progression by enhancing the JNK and ERK signaling pathway. Hep-3B cells were transfected with LAGE3-OE and then incubated with ERK inhibitor SCH772984 or JNK inhibitor SP600125. A Western blot bands of p-p38, p38, p-JNK, JNK, p-ERK, and ERK in Hep3B cells. B Proliferation ability of Hep3B cells. C–D Migration and invasion abilities of Hep3B cells. Data are shown as mean ± standard deviation. *p < 0.05, **p < 0.01

7). Melatonin restores endoplasmic reticulum homeostasis to protect injured neurons in a rat model of chronic cervical cord compression. JOURNAL OF PINEAL RESEARCH, 2023 (PubMed: 36732085) [IF=8.3]

8). N6-methyladenosine Reader IGF2BP2-modified HMMR Promotes Non-small Cell Lung Cancer Metastasis via Interaction with MAP4K4. International journal of biological sciences, 2025 (PubMed: 39990663) [IF=8.2]

9). LncRNA CD27-AS1 promotes acute myeloid leukemia progression through the miR-224-5p/PBX3 signaling circuit. Cell Death & Disease, 2021 (PubMed: 34006845) [IF=8.1]

Application: WB    Species: Human    Sample: AML cells

Fig. 5 CD27-AS1 regulates MAPK signaling pathway in the AML cell lines. a HL-60 and KG-1 cells were infected with LV-CD27-AS1 and LV-CD27- AS1-Sh1. Protein levels of P38, p-P38, JNK, p-JNK, p-C-raf, p-MEK1/2, ERK, and p-ERK were detected using western blotting. b Densitometry analysis of protein levels in both cells was performed. c U0126, a MEK1/2 inhibitor, was used to treat the AML cells with CD27-AS1 upregulation. Relative protein levels of p-ERK and ERK were measured using western blotting. d CCK-8 assay was performed to check cell viability. N = 3. Data were shown as means ± SD. *P < 0.05, **P < 0.01, and ***P < 0.001.

10). IL-37b alleviates endothelial cell apoptosis and inflammation in Kawasaki disease through IL-1R8 pathway. Cell Death & Disease, 2021 (PubMed: 34083516) [IF=8.1]

Application: WB    Species: Mouse    Sample: endothelial cells

Fig. 5 IL-37b inhibited the activation of ERK and NFκB in KD-treated ECs related to IL-1R8. a Effects of IL-37b treatment on the phosphorylation of ERK, JNK, p38, and NFκB p65 were assessed in the treated endothelial cells. b–e Quantitative analysis of these above proteins was conducted. Data are presented as mean ± SD (n = 3). Significance: *P < 0.05 vs. the HC group, and #P < 0.05 vs. the KD group. f, g Effects of IL-1R8 silencing on the activation of ERK and NFκB p65 were observed. Significance: *P < 0.05 vs. the HC group, #P < 0.05 vs. the KD group, and &P < 0.05 vs. the KD + IL-37b group. i The nuclear translocation of NFκB p65 was observed after silencing IL-1R8 expression (n = 3). Magnification: ×200, Scale bar = 100 μm. Experiments were done at least three times in triplicate.

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