Kinetic formulation of the effect stands ready to be integrated into the expanding thermodynamic description of the GPCR system at large (Kenakin, 2010). From a practical point of view, the availability of naturally occurring pluridimensional effects suggests it should be possible to fine-tune the therapeutic action of a GPCR drug beyond the simple margins traditionally dictated by the target's ti

Nal peptide (SignalP 3.0), transmembrane domains (transmembrane helices by hidden Markov model), and PEXEL motif. The transcript levels of cognate genes were derived from the DeRisi and co-worker (15) transcriptome data, orthologs were from the Plasmodium database (16), and genome-wide polymorphism data were obtained from a study by Mu et al. (17). Protein function was assigned based on published

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Tumors, such as COL1A1, COL4A1, FN1, LOXL1, TGFBI, TNC, and VIM. Furthermore, annexins (ANXA1, ANXA2, and ANXA5), which are also membrane proteins, were detected. Additionally, several metabolic enzymes were detected, including glycolytic enzymes (aldolase A, fructose-bisphosphate; aldolase C, fructose-bisphosphate; enolase 2; GAPDH; LDHA; LDHAL68; PKM2; and TPI). It is of note that the tumor-spec

Utant that we had earlier observed associating with ESCRT-I, the YLPM1 associated proteins, and CPSF6/7. When we purified Halo-TNIP2 196 ?46 associated proteins in the presence of Benzonase? an endonuclease that digests both DNA and RNA, we detected the bait proteins shown in Fig. 5A (light gray bars). There was no significant change in the relative amounts of the subunits of the ESCRT-I complex d

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