By Charles Kliment, Don Greer
Information the German half-track and its versions from international conflict II
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Extra resources for SdKfz 251 in action
To clarify this issue, the SOS phosphorylating activity was resolved from ERK activity by expression of the MAP kinase specific phosphatase, MKPI. Furthermore, physical separation of ERK activity from another MEK-dependent kinase activity was achieved by FPLC anion exchange chromatography . These data directly demonstrated the presence of a SOS kinase activity in CHO cells which is distinct from the ERK activity. However, this apparent feedback pathway for Ras inactivation is not universal, as other mechanisms for Ras desensitization appear to be present .
Steps in signalling by the sevenless proteins tyrosine lmase. Cell 87: 701-718,1991 Bowtell D, Fu P, Simon M, Senior P: Identitication of munne homologues of the Drosophila son of sevenless gene: Potential activators of Ras. Proc Natl AcadSci USA 89: 6511-6515,1992 Myers MG Jr, White MF: Insulin signal transducti('11 and the IRS proteins. Ann Rev Pharm Toxicol 36: 615-658, 1996 Waters SB, Pessin lE: Insulin receptor substrate 1 and 2 (IRS I and IRS2): What a tangled web we weave. Trends Cell BioI 6: 1-4, 1996 Myers MG lr, Wang L-M, Sun Xl, Zhang Y, Yenush L.
Insulin receptor activation results in the GTP-charging of Ras which creates a high affinity ligand for the protein kinases of the Raf family. Once bound to Ras at the membrane, Raf undergoes further modification by one of several (SerlThr) or (Tyr) kinases, depending on the initiating stimulus. Insulin receptor activation also activates PI-3 kinase, which generates a variety of 3-0H phosphorylated Ptd Ins derivatives, each of which acts as a binding partner for a variety of protein kinases, including some PKC isoforms.