PathScan® Inflammation Multi-Target Sandwich ELISA Kit #7276
- ELISA+
Inquiry Info. # 7276
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Product Specifications
| REACTIVITY | H M |
Application Key:
- ELISA+-ELISA and/or ELISA-like Assays
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
Product Information
Product Description
实验步骤
Specificity / Sensitivity
Species Reactivity:
Background
The stress-activated protein kinase/Jun-amino-terminal kinase SAPK/JNK is 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 (5-10). As with the other MAPKs, the core-signaling unit is composed of a MAPKKK, typically MEKK1-4, or by a mixed lineage kinase (MLK), which phosphorylates and activates MKK4-7, which then phosphorylates Thr183 and Tyr185 to activate the SAPK/JNK kinase (6). Stress signals are delivered to this cascade by small GTPases of the Rho family (Rac, Rho, cdc42) (7). Both Rac1 and cdc42 mediate the stimulation of MEKKs and MLKs (7). Alternatively, MKK4-7 can be activated by a pathway independent of small GTPases via stimulation of a member of the germinal center kinase (GCK) family (8).
p38 MAP kinase (MAPK) participates in a signaling cascade controlling the cellular response to pro-inflammatory cytokines and a variety of cellular stresses. MKK3, MKK6 and SEK (MKK4) activate p38 MAP kinase by phosphorylation at Thr180 and Tyr182 (11-14).
The Stat3 transcription factor is an important signaling molecule for many cytokines and growth factor receptors. Stat3 is activated by phosphorylation at Tyr705, which induces dimerization, nuclear translocation and DNA binding (15,16).
- Ghosh, S. and Karin, M. (2002) Cell 109 Suppl, S81-96.
- DiDonato, J. et al. (1996) Mol Cell Biol 16, 1295-304.
- Sakurai, H. et al. (1999) J Biol Chem 274, 30353-6.
- Mattioli, I. et al. (2004) J Immunol 172, 6336-44.
- Davis, R.J. (1999) Biochem Soc Symp 64, 1-12.
- Ichijo, H. (1999) Oncogene 18, 6087-93.
- Kyriakis, J.M. and Avruch, J. (2001) Physiol Rev 81, 807-69.
- Kyriakis, J.M. (1999) J Biol Chem 274, 5259-62.
- Leppä, S. and Bohmann, D. (1999) Oncogene 18, 6158-62.
- Whitmarsh, A.J. and Davis, R.J. (1998) Trends Biochem Sci 23, 481-5.
- Raingeaud, J. et al. (1995) J Biol Chem 270, 7420-6.
- Raman, M. et al. (2007) Oncogene 26, 3100-12.
- Zarubin, T. and Han, J. (2005) Cell Res 15, 11-8.
- Roux, P.P. and Blenis, J. (2004) Microbiol Mol Biol Rev 68, 320-44.
- O'Shea, J.J. et al. (2002) Cell 109 Suppl, S121-31.
- Kaptein, A. et al. (1996) J Biol Chem 271, 5961-4.
Alternate Names
Acute-phase response factor; ADMIO; ADMIO1; APRF; c-Jun N-terminal kinase 1; CMCU; CSAID-binding protein; Csaids binding protein; CSBP; CSBP1; CSBP2; CSPB1; cytokine suppressive anti-inflammatory drug binding protein; Cytokine suppressive anti-inflammatory drug-binding protein; DNA-binding protein APRF; EDAID2; EXIP; FLJ20882; HIES; I-kappa-B-alpha; IkappaBalpha; IkB-alpha; IKBA; JNK; JNK-46; JNK1; JNK1 alpha protein kinase; JNK1 beta protein kinase; JNK1A2; JNK21B1/2; JUN N-terminal kinase; MAD-3; MAD3; Major histocompatibility complex enhancer-binding protein MAD3; MAP kinase 14; MAP kinase 8; MAP kinase MXI2; MAP kinase p38 alpha; MAPK 14; MAPK 8; MAPK14; MAPK8; MAX-interacting protein 2; MGC131774; MGC16063; Mitogen-activated protein kinase 14; 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 p38 alpha; MK08; MK14; MXI2; NF-kappa-B inhibitor alpha; NF-kappa-B p65delta3; NF-kappa-B transcription factor p65; NFKB inhibitor alpha; NFkB-p65; NFKB3; NFKBI; NFKBIA; Nuclear factor NF-kappa-B p65 subunit; nuclear factor of kappa light chain gene enhancer in B-cells; Nuclear factor of kappa light polypeptide gene enhancer in B-cells 3; nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha; p38; p38 MAP kinase; p38 mitogen activated protein kinase; p38-alpha; P38A; p38ALPHA; p38alpha Exip; p65; PRKM14; PRKM15; PRKM8; protein kinase JNK1; RELA; RELA proto-oncogene, NF-kB subunit; RELA/p65; RK; SAPK1; SAPK1C; SAPK2A; Signal transducer and activator of transcription 3; signal transducer and activator of transcription 3 (acute-phase response factor); STAT3; Stress-activated protein kinase 1; Stress-activated protein kinase 1c; stress-activated protein kinase 2A; Stress-activated protein kinase JNK1; TF65; Transcription factor p65; v-rel avian reticuloendotheliosis viral oncogene homolog A; v-rel avian reticuloendotheliosis viral oncogene homolog A (nuclear factor of kappa light polypeptide gene enhancer in B-cells 3 (p65)); v-rel reticuloendotheliosis viral oncogene homolog A (avian); v-rel reticuloendotheliosis viral oncogene homolog A, nuclear factor of kappa light polypeptide gene enhancer in B-cells 3, p65
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