Cell Signaling Technology

Product Pathways - MAPK Signaling

Phospho-SAPK/JNK (Thr183/Tyr185) (G9) Mouse mAb #9255

JNK   SAPK   SAPK3   sc-6254   stress-activated-protein-kinase  

No. Size Price
9255L 600 µl ( 120 western blots ) ¥8,992.00 现货查询 购买询价 防伪查询
9255S 200 µl ( 40 western blots ) ¥3,960.00 现货查询 购买询价 防伪查询
9255 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:2000 Human,Mouse,Rat,Hamster,S. cerevisiae, Endogenous 46, 54 Mouse IgG1
IP 1:250
F 1:400
IF-IC 1:400

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting, IP=Immunoprecipitation, F=Flow Cytometry, IF-IC=Immunofluorescence (Immunocytochemistry),

Specificity / Sensitivity

Phospho-SAPK/JNK (Thr183/Tyr185) (G9) Mouse mAb detects endogenous levels of p46 and p54 SAPK/JNK dually phosphorylated at Thr183 and Tyr185. This antibody does not recognize endogenous levels of phosphorylated p44/42 MAPK or p38 MAP kinase.

Phospho-SAPK/JNK (Thr183/Tyr185) (G9) Mouse mAb鼠单抗能够检测内源性Thr183/Tyr185位点磷酸化的p46 、p54 SAPK/JNK蛋白水平。该抗体不能识别磷酸化的p44/42、p38 MAP激酶。

Source / Purification

Monoclonal antibody is produced by immunizing mice with a synthetic phosphopeptide corresponding to residues surrounding Thr183/Tyr185 of human SAPK/JNK.


Western Blotting

Western Blotting

Western blot analysis of extracts from 293 cells, untreated or UV-treated (lanes 1 and 2), NIH/3T3 cells, untreated or UV-treated (lanes 3 and 4) and C6 cells, untreated or anisomycin-treated (lanes 5 and 6), using Phospho-SAPK/JNK (Thr183/Tyr185) (G9) Mouse mAb.western blot方法检测细胞提取物:未处理和紫外照射的293 细胞(1、2号条带),未经处理的和紫外照射的COS细胞(3、4号条带),未处理和茴香霉素处理的C6细胞(5、6号条带)。使用的抗体是Phospho-SAPK/JNK (Thr183/Tyr185) (G9) Mouse mAb。

Flow Cytometry

Flow Cytometry

Flow cytometric analysis of Jurkat cells, untreated (green) or anisomycin-treated (blue), using Phospho-SAPK/JNK (Thr183/Tyr185) (G9) Mouse mAb compared to a nonspecific negative control antibody (red).流式细胞方法检测未处理(绿色)和茴香霉素处理(蓝色)的Jurkat细胞。使用抗体为Phospho-SAPK/JNK (Thr183/Tyr185) (G9) Mouse mAb,红色为非特异结合的阴性对照。



Confocal immunofluorescent analysis of HeLa cells untreated (left) and anisomycin-treated (right) using Phospho-SAPK/JNK (Thr183/Tyr185) (G9) Mouse mAb (green). Actin filaments have been labeled with DY554 phalloidin (red).激光共聚焦荧光法检测HeLa细胞,左图为未处理的,右图为茴香霉素处理的,检测抗体为Phospho-SAPK/JNK (Thr183/Tyr185) (G9) Mouse mAb ,呈绿色。肌动蛋白丝被DY-554鬼笔环肽标记,呈红色。


The stress-activated protein kinase/Jun-amino-terminal kinase SAPK/JNK is potently and preferentially activated by a variety of environmental stresses including UV and gamma radiation, ceramides, inflammatory cytokines, and in some instances, by growth factors and GPCR agonists (1-6). As with the other MAPKs, the core signaling unit is composed of a MAPKKK, typically MEKK1-MEKK4, or by one of the mixed lineage kinases (MLKs), which phosphorylate and activate MKK4/7. Upon activation, MKKs phosphorylate and activate the SAPK/JNK kinase (2). Stress signals are delivered to this cascade by small GTPases of the Rho family (Rac, Rho, cdc42) (3). Both Rac1 and cdc42 mediate the stimulation of MEKKs and MLKs (3). Alternatively, MKK4/7 can be activated in a GTPase-independent mechanism via stimulation of a germinal center kinase (GCK) family member (4). There are three SAPK/JNK genes each of which undergoes alternative splicing resulting in numerous isoforms (3). SAPK/JNK, when active as a dimer, can translocate to the nucleus and regulate transcription through its effects on c-Jun, ATF-2, and other transcription factors (3,5).

应激活化蛋白激酶/Jun氨基末端激酶SAPK/JNK能够有效、优先地被多种环境压力激活,这些环境压力包括紫外照射和gamma 辐射、神经酰胺、炎性因子,在某些情况下也包括生长因子和GPCR激动剂 (1-6)。正如其他的 MAPKs,核心信号传导单元包括一个MAPKKK,通常是MEKK1-MEKK4,或一种混合谱系酶 (MLKs),这些MAPKKK激酶能磷酸化并激活 MKK4/7。活化后,MKKs磷酸化并激活SAPK/JNK 激酶 (2)。应激反应信号经Rho 家族(Rac, Rho, cdc42)的小GTP酶被传递到这个级联信号反应中 (3)。Rac1 和 cdc42蛋白都能调节MEKKs、 MLKs的激活(3)。另外一种情况是,MKK4/7能够通过生发中心激酶 (GCK)家族成员的刺激,在一个非GTP酶依赖机制中被激活 (4)。有三种不同的SAPK/JNK基因,而每一种都会经过选择性剪切产生多种异构体(3)。活化的二聚体SAPK/JNK,能转位到细胞核中,通过它对 c-Jun, ATF-2和其他转录因子的效应而调节转录过程(3,5)。

  1. Davis, R.J. (1999) Biochem Soc Symp 64, 1-12.
  2. Ichijo, H. (1999) Oncogene 18, 6087-93.
  3. Kyriakis, J.M. and Avruch, J. (2001) Physiol Rev 81, 807-69.
  4. Kyriakis, J.M. (1999) J Biol Chem 274, 5259-62.
  5. Leppä, S. and Bohmann, D. (1999) Oncogene 18, 6158-62.
  6. Whitmarsh, A.J. and Davis, R.J. (1998) Trends Biochem Sci 23, 481-5.

Application References

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