Phospho-TAK1 (Thr187) Antibody - #AF3019

>>买2送1 进行中>>
>>赠JD卡 进行中>>
(7)   (15)  
产品: 磷酸化 TAK1 (Thr187) 抗体
货号: AF3019
描述: Rabbit polyclonal antibody to Phospho-TAK1 (Thr187)
应用: WB IHC IF/ICC
文献验证: WB
反应: Human, Mouse, Rat
预测: Zebrafish, Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
蛋白号: O43318
RRID: AB_2832996

浏览相似产品>>

   规格 价格 库存
 50ul RMB¥ 1300 现货
 100ul RMB¥ 2400 现货
 200ul RMB¥ 3200 现货

货期: 当天发货

联系销售
相关下载
MSDS
说明书
COA
实验方案
WB Handbook
IHC Protocol
IF/ICC Protocol

产品描述

来源:
Rabbit
应用:
WB 1:500-1:2000, IHC 1:50-1:500, 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-TAK1 (Thr187) Antibody detects endogenous levels of TAK1 only when phosphorylated at Threonine 187.
RRID:
AB_2832996
引用格式: Affinity Biosciences Cat# AF3019, RRID:AB_2832996.
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

M3K7_HUMAN; MAP3K 7; Map3k7; MEKK7; Mitogen activated protein kinase kinase kinase 7; Mitogen-activated protein kinase kinase kinase 7; TAK1; TGF beta activated kinase 1; TGF-beta-activated kinase 1; TGF1a; Transforming growth factor beta activated kinase 1; Transforming growth factor-beta-activated kinase 1;

抗原和靶标

免疫原:

A synthesized peptide derived from human TAK1 around the phosphorylation site of Thr187.

基因/基因ID:
MAP3K7(6885)
描述:
AK1 a protein kinase of the MLK family. Mediates signal transduction induced by TGF beta and morphogenetic protein (BMP), and controls a variety of cell functions including transcription regulation and apoptosis. In response to IL-1, forms a kinase complex including TRAF6, MAP3K7P1/TAB1 and MAP3K7P2/TAB2; this complex is required for the activation of nuclear factor kappa B.

研究领域

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

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

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

· Environmental Information Processing > Signal transduction > NF-kappa B signaling pathway.   (View pathway)

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

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

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

· Human Diseases > Infectious diseases: Parasitic > Leishmaniasis.

· Human Diseases > Infectious diseases: Parasitic > Toxoplasmosis.

· Human Diseases > Infectious diseases: Viral > Measles.

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

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

· 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 > T cell receptor signaling pathway.   (View pathway)

文献引用

1). TRAF3 mediates neuronal apoptosis in early brain injury following subarachnoid hemorrhage via targeting TAK1-dependent MAPKs and NF-κB pathways. Cell Death & Disease, 2021 (PubMed: 33414375) [IF=8.1]

Application: WB    Species: Human    Sample: neural cells

Fig. 7 TRAF3–TAK1 interaction and phosphorylation of TAK1 are required for TRAF3-dependent neuronal apoptosis in SAH. Western blot analysis revealed that TRAF3 siRNA reduced the phosphorylation of TAK1 after SAH both in vivo (A, B) and in vitro (C, D). N = 6 mice or wells per group. *p 
2). Cerebral endothelial cell-derived extracellular vesicles regulate microglial polarization and promote autophagy via delivery of miR-672-5p. Cell death & disease, 2023 (PubMed: 37773169) [IF=8.1]
3). SHP-1 suppresses endotoxin-induced uveitis by inhibiting the TAK1/JNK pathway. Journal of Cellular and Molecular Medicine, 2021 (PubMed: 33207073) [IF=5.3]

Application: WB    Species: Rat    Sample: rMC‐1 cells

FIGURE 7 SHP‐1 negatively regulates kinase phosphorylation in LPS‐treated rMC‐1 cells. A, Effects of SHP‐1 overexpression on inflammatory signalling pathways. Blank‐rLV‐ and SHP‐1‐rLV‐ transfected rMC‐1 cells were exposed to 10 μg/mL LPS for 0, 15 or 30 min, and Western blotting was performed to determine the phosphorylation status of TAK1, JNK and NF‐κB and the total protein levels of JNK and NF‐κB. B‐D, Quantitative analysis of pTAK1/β‐actin (B), pJNK/JNK (C) and pNF‐κB/NF‐κB (D). E, Effects of SHP‐1 knockdown on inflammatory signalling pathways. Blank‐rLV‐ and shRNA‐SHP‐1‐rLV‐transfected rMC‐1 cells were exposed to 10 μg/mL LPS for 0, 15, or 30 min, and Western blotting was performed to determine the phosphorylation status of TAK1, JNK and NF‐κB and the total protein levels of JNK and NF‐κB. F‐H, Quantitative analysis of pTAK1/β‐actin (F), pJNK/JNK (G) and pNF‐κB/NF‐κB (H). Two‐way ANOVA followed by Dunnett's test was used. n = 3 per group. *P < .05 and **P < .01
4). Kongensin a attenuates intervertebral disc degeneration by inhibiting TAK1-mediated PANoptosis of nucleus pulposus cells. International immunopharmacology, 2024 (PubMed: 38359662) [IF=4.8]

Application: WB    Species: Rat    Sample: NPCs

Fig. 3. Biobehavioral differences induced by KA treatment of NPCs. a Volcano plot presenting 20 upregulated and 78 downregulated DEGs in RNA-seq analysis. b-d GO enrichment results showed that most DEGs were involved in response to oxidative stress, ROS and regeneration. e KEGG enrichment analysis was used to study pathways that may be involved in the treatment process. f, g Effects of KA on TAK1 and p-TAK1 expression (n = 3).
5). Axonal injury mediated by neuronal p75NTR/TRAF6/JNK pathway contributes to cognitive impairment after repetitive mTBI. Experimental neurology, 2024 (PubMed: 38029807) [IF=4.6]
6). TAK1 Reduces Surgery-induced Overactivation of RIPK1 to Relieve Neuroinflammation and Cognitive Dysfunction in Aged Rats. Neurochemical Research, 2023 (PubMed: 37329446) [IF=3.7]

Application: WB    Species: Rat    Sample: hippocampal

Fig. 3 TAK1 inhibition exacerbated neuroinflammation and cognitive dysfunction in young rats after surgery, which were reversed by a RIPK1 inhibitor. (a-b) Comparison of the total distance travelled by the rats in the OFT at different time points. (c) The percentage of freezing time at 72 h after surgery. (d-e) Representative western blots and analysis of TAK1, pTAK1, RIPK1 and pRIPK1 expression at 72 h after surgery. (f-i) Representative western blots and analysis of TNF-α, pro-IL-1β, AP-1 and NF-κB p65 expression in hippocampal samples 72 h after surgery. (j) Quantification of GFAP and Iba1 fluorescence in the hippocampal CA1 region 72 h after surgery. (k) Representative images of GFAP and Iba1 fluorescence in the hippocampal CA1 region 72 h after surgery. The data are presented as the mean ± SD (n = 10).
7). Anemarsaponin B mitigates acute pancreatitis damage in mice through apoptosis reduction and MAPK pathway modulation.. Biocell, 2024 [IF=0.8]

限制条款

产品的规格、报价、验证数据请以官网为准，官网链接：www.affbiotech.com | www.affbiotech.cn（简体中文）| www.affbiotech.jp（日本語）

产品的数据信息为Affinity所有，未经授权不得收集Affinity官网数据或资料用于商业用途，对抄袭产品数据的行为我们将保留诉诸法律的权利。

产品相关数据会因产品批次、产品检测情况随时调整，如您已订购该产品，请以订购时随货说明书为准，否则请以官网内容为准，官网内容有改动时恕不另行通知。

Affinity保证所销售产品均经过严格质量检测。如您购买的商品在规定时间内出现问题需要售后时，请您在Affinity官方渠道提交售后申请。

产品仅供科学研究使用。不用于诊断和治疗。 

产品未经授权不得转售。

Affinity Biosciences将不会对在使用我们的产品时可能发生的专利侵权或其他侵权行为负责。Affinity Biosciences, Affinity Biosciences标志和所有其他商标所有权归Affinity Biosciences LTD.