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RAS Pathway Assay (CAT#: STEM-MB-0350-WXH)

Introduction

The RAS proteins control signalling pathways that are key regulators of several aspects of normal cell growth and malignant transformation. They are aberrant in most human tumours due to activating mutations in the RAS genes themselves or to alterations in upstream or downstream signalling components. Rational therapies that target the RAS pathways might inhibit tumour growth, survival and spread.




Principle

Normally, Ras combines with GDP and is in an inactive state. When Ras protein is released from Ras/GDP and binds to GTP, Ras is activated. Guanylate exchange factors (GEFs) (e.g. Sos) are stimuli for the activation of Ras. GAP (GTPase activating proteins) catalyzing the hydrolysis of GTP to GDP in Ras/GTP, deactivating Ras.
Active Ras binds and activates Raf. Activated Raf phosphorylates and activates MEK1/2. MEK 1/2 phosphorylates ERK1/2 to activate it. Activation of ERK1/2 into the nucleus activates the expression of many downstream genes such as Elk-1, elf-4E to promote cell proliferation and differentiation.

Applications

To study the effect of each virus on RAS signaling pathway
To study the regulation mechanism of RAS signal pathway in disease
To study the effects of drugs or therapies on RAS signaling pathways

Procedure

• Luminex Multiplex Assay
• Enzyme-linked immunosorbent assay (ELISA)
• Flow cytometry (FACS analysis) technology

Notes

Detectable targets: NMDAR, GPCR, TCR, GF, RTK, CaM, PKA, Gβy, ZAP70, PLSy, SHC, SHP2, Grb2, Gab, Ras, SOS, LAT, NF1, GRFs, RLIP76, Arg6, Rac1, RINI, RAB5, ABL, PLCE, PKC, RGL2, CDC42, RGL, PLD, JNK, TBK1, NF-kB, Sec5, Rap1, Repac, AF6, KSP, Raf-1, MEK, ERK, ETS, ELK, PLA, FasL, BCL-X, AFXIKK, IKK, Rho, Rac, Akt, PKB, PAK, TIAMI, Mst1, Nore1, RASSF1,

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