Phospho-ASK1 (Ser966) Antibody - #AF3477

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产品: 磷酸化 ASK1 (Ser966) 抗体
货号: AF3477
描述: Rabbit polyclonal antibody to Phospho-ASK1 (Ser966)
应用: WB IHC IF/ICC
文献验证: WB, IF/ICC
反应: Human, Mouse, Rat
预测: Pig, Zebrafish, Bovine, Horse, Sheep, Rabbit, Dog, Chicken
蛋白号: Q99683
RRID: AB_2834915

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产品描述

来源:
Rabbit
应用:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human, Mouse, Rat
克隆:
Polyclonal
特异性:
Phospho-ASK1 (Ser966) Antibody detects endogenous levels of ASK1 only when phosphorylated at Serine 966.
RRID:
AB_2834915
引用格式: Affinity Biosciences Cat# AF3477, RRID:AB_2834915.
偶联:
Unconjugated.
纯化:
The antibody is from purified rabbit serum by affinity purification via sequential chromatography on phospho-peptide and non-phospho-peptide affinity columns.
保存:
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.
别名:

展开/折叠

Apoptosis signal regulating kinase 1; Apoptosis signal-regulating kinase 1; ASK 1; ASK-1; ASK1; M3K5; M3K5_HUMAN; MAP/ERK kinase kinase 5; MAP3K5; MAPK/ERK kinase kinase 5; MAPKKK5; MEK kinase 5; MEKK 5; MEKK5; Mitogen activated protein kinase kinase kinase 5; Mitogen-activated protein kinase kinase kinase 5;

抗原和靶标

免疫原:

A synthesized peptide derived from human ASK1 around the phosphorylation site of Ser966.

基因/基因ID:
MAP3K5(4217)
描述:
Mitogen-activated protein kinase (MAPK) signaling cascades include MAPK or extracellular signal-regulated kinase (ERK), MAPK kinase (MKK or MEK), and MAPK kinase kinase (MAPKKK or MEKK). MAPKK kinase/MEKK phosphorylates and activates its downstream protein kinase, MAPK kinase/MEK, which in turn activates MAPK.

研究领域

· Cellular Processes > Cell growth and death > Apoptosis.   (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 > Sphingolipid 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 > Platinum drug resistance.

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

· Human Diseases > Neurodegenerative diseases > Amyotrophic lateral sclerosis (ALS).

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

文献引用

1). FUT2-dependent fucosylation of HYOU1 protects intestinal stem cells against inflammatory injury by regulating unfolded protein response. Redox biology, 2023 (PubMed: 36724577) [IF=10.7]

Application: WB    Species: Mouse    Sample:

Fig. 7. Restraint of LPS-stimulated UPR initiation via IRE1/TRAF2/ASK1/JNK branch by fucose. (A) The relative mRNA expression of UPR-related molecules, including Grp78, Atf6, Atf4, Chop, Xbp1s, Traf2, and Txnip in intestinal organoids treated with LPS and FUC. (B) Immunofluorescence staining of GRP78 in intestinal organoids for each group. Scale bar: 100 μm. (C) Western blot analysis of IRE1 signaling related proteins in the UPR branch. (D) Densitometric analysis of IRE1 signaling-related proteins was shown in the statistical chart. The activation of IRE1, ASK1, and JNK was assessed by calculating the ratio of phosphorylated protein to total protein. The expression of TRAF2 was normalized to ACTB. (E) Western blot analysis of ATF6, ATF4, and CHOP in the UPR branch. (F) Densitometric analysis of ATF6, ATF4, and CHOP in organoids was shown in the statistical chart. At least 3 independent experiments were conducted. Results were shown as mean ± SD. ns, non-significant; *P < 0.05, *P < 0.01, ***P < 0.001.
2). ASK1-K716R reduces neuroinflammation and white matter injury via preserving blood-brain barrier integrity after traumatic brain injury. Journal of neuroinflammation, 2023 (PubMed: 37875988) [IF=9.3]

Application: IF/ICC    Species: Mouse    Sample:

Fig. 2 ASK1-K716R inhibits the activation of ASK1/JNKs signaling pathway and protects tight junction proteins in extracted brain microvessels. A–C Representative Western blot bands (A) and quantification (B, C) of p-ASK1/ASK1, p-JNKs/JNKs, p-p38/p38 in extracted brain microvessels (n = 4/group). D Representative images of endothelial cells (CD31+) expressing p-ASK1, p-JNKs, and p-p38 at peri-lesion cortex 3 days following TBI. Scale bar, 20 μm. E Representative images and quantification of TUNEL+ (red) and CD31+ (green) staining at peri-lesion cortex 3 days following TBI. n = 6 for WT TBI, n = 5 for ASK1-K716R TBI. Scale bar, 20 μm. F, G Representative Western blot bands (F) and quantification (G) of Occludin and VE-Cadherin in extracted brain microvessels. n = 4/group. All data from male mice are presented as the mean ± SD. One-way ANOVA test and Bonferroni post hoc (B, C, F, G) and Student’s t test (E). * p 
3). Targeting Notch1-YAP Circuit Reprograms Macrophage Polarization and Alleviates Acute Liver Injury in Mice. Cellular and Molecular Gastroenterology and Hepatology, 2023 (PubMed: 36706917) [IF=7.1]

Application: WB    Species: Mouse    Sample:

Figure 3 Myeloid-specific deletion of Notch1 alleviates LPS/D-GalN-induced hepatocellular apoptosis. (A) Representative TUNEL staining images and quantification of TUNEL+ cells in liver sections from the Notch1FL/FL and Notch1M-KO mice treated with PBS or LPS/D-GalN injection (n = 5 mice/group). Scale bars, 20 μm. (B) Immunohistochemistry staining and quantification of cleaved caspase-3 (C-caspase-3) positive cells in liver sections (n = 5 mice/group). Scale bars, 40 μm. ELISA analysis of serum TNF-α (C) and HMGB1 (D) levels in the Notch1FL/FL and Notch1M-KO mice (n = 5 samples/group). (E) Western blot analysis and relative density ratio of p-ASK1, ASK1, p-p38, p38, C-caspase-3, caspase-3, Bcl-xL, and Bax in the Notch1FL/FL and Notch1M-KO livers. Data are presented as the mean ± standard deviation. ∗P < .05, ∗∗P < .01.
4). Dual function of peroxiredoxin I in lipopolysaccharide-induced osteoblast apoptosis via reactive oxygen species and the apoptosis signal-regulating kinase 1 signaling pathway. Cell Death Discovery, 2018 (PubMed: 29707240) [IF=7.0]

Application: WB    Species:    Sample: Wild-type, Prx1KO, and Prx1OE cells

Fig. 6 |The overexpression of Prx1 promotes ASK1 activation by inhibiting the activity of Trx towards ASK1. a–d Wild-type, Prx1KO, and Prx1OE cells were each divided into three groups, which were control groups, groups treated with 100 ng/ml LPS, and groups treated with 100 ng/ml LPS and NQDI. Western blot analysis was then performed with antibodies against P-ASK1, ASK1, Trx and GAPDH.
5). JNK signaling pathway mediates acetaminophen-induced hepatotoxicity accompanied by changes of glutathione S-transferase A1 content and expression. Frontiers in Pharmacology, 2019 (PubMed: 31620005) [IF=5.6]

Application: WB    Species: mouse    Sample: liver

FIGURE 2 | Activation of JNK signaling pathway under different dosages of APAP. .(E) Western blot analyses of total tissue lysate for p-ASK1, ASK1, p-MKK4, MKK4, and β-actin (loading control). Values represented as means ± SD, n = 3. *Represents statistical differences caused by APAP. #Represents statistical differences caused by SP600125 under 150 mg·kg−1 APAP;§Represents statistical differences caused by SP600125 under 175 mg·kg−1 APAP. 0.05 > P > 0.01 (*, #, §). P < 0.01 (**, §§).
6). Byakangelicin protects against carbon tetrachloride–induced liver injury and fibrosis in mice. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, 2020 (PubMed: 32643868) [IF=5.3]

Application: WB    Species: human    Sample: LX-2 cells

FIGURE 5|Byakangelicin inhibits 4-HNE–induced hepatocyte apoptosis by inhibiting ASK1/JNK pathway. D and E, Protein full-length PARP, PARP, cleaved caspase-3, caspase-3, JNK, P-JNK, ASK-1 and P-ASK-1 were also detected and quantified using Western blot analyses.
7). Inhibition of Endoplasmic Reticulum Stress Improves Chronic Ischemic Hippocampal Damage Associated with Suppression of IRE1α/TRAF2/ASK1/JNK-Dependent Apoptosis. Inflammation, 2024 (PubMed: 38401021) [IF=4.5]

Application: WB    Species: Rat    Sample:

Fig. 5 Effects of 4-PBA and URB597 on TRAF2/ASK/JNK signaling. a Representative images of p-ASK1 (green) immunofluorescence. b Statistical analysis of the relative fluorescence intensity. c Co-IP experiment between TRAF2 and ASK1. d Representative Western blots of the ASK/JNK signaling-related proteins ASK1, p-ASK1, JNK1/2/3, and p-JNK1/2/3. e, f Relative protein expression levels. *P 
8). CTGF Triggers Rat Astrocyte Activation and Astrocyte-Mediated Inflammatory Response in Culture Conditions. INFLAMMATION, 2019 (PubMed: 31183597) [IF=4.5]

Application: WB    Species: rat    Sample: RA cells

Fig. 4.| CTGF activated the NF-κB and AP-1 through ASK1-p38/JNK pathways. b RA cells were treated with either 10 μM ASK1 inhibitor GS-4997, or solvent control as indicated, for 30 min prior to stimulation with 20 ng/ml CTGF for 24 h. The expression of ASK, p65, and c-Jun and their phosphorylation states were examined by Western blotting.

Application: WB    Species: rat    Sample: RA cells

Fig. 4.| CTGF activated the NF-κB and AP-1 through ASK1-p38/JNK pathways. b RA cells were treated with either 10 μM ASK1 inhibitor GS-4997, or solvent control as indicated, for 30 min prior to stimulation with 20 ng/ml CTGF for 24 h. The expression of ASK, p65, and c-Jun and their phosphorylation states were examined by Western blotting.
9). Rosmarinic acid attenuates acrylamide induced apoptosis of BRL-3A cells by inhibiting oxidative stress and endoplasmic reticulum stress. Food and Chemical Toxicology, 2021 (PubMed: 33781805) [IF=3.9]

Application: WB    Species: Mouse    Sample: BRL-3A cells

Fig. 4. The effect of AA, RosA and NAC on ERS in BRL-3A cells. DMEM basic medium, RosA (6.25, 12.5, 25, 50 μM) and 10 mM NAC were used for pretreatment for 2 h, incubated with 2 mM AA for 24 h. (A) The effect of AA and RosA on the release of calcium ions in BRL-3A cells. (B) The effect of AA and RosA on IRE1α pathway signal proteins. (C) The effect of AA and RosA on ERS-mediated apoptosis-related proteins. (D) The effect of NAC on ERS-related proteins in BRL-3A cells. Western blotting analysis showed the protein levels of p-IRE1α, IRE1α, GRP78, XBP-1s, TRAF2, p-ASK1, Caspase-12, and CHOP in BRL-3A cells. Values are expressed as mean ± standard deviation (n = 3). Compared with the control group, **P < 0.01; compared with the AA group, #P < 0.05 and ##P < 0.01.
10). Elaidic acid induced NLRP3 inflammasome activation via ERS-MAPK signaling pathways in Kupffer cells. BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS, 2022 (PubMed: 34610469) [IF=3.9]
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