Match the protein on the left with the mechanism of how the protein is activated on the right. Beclin-1 XBP-15 Rheb LC3 IRE-1 [Choose] [Choose] Phosphorylation Binding another protein to form a complex Dephosphorylation Cleavage Binding of GTP Dimerization Splicing in cytoplasm [Choose] [Choose]

Which of the following small GTP-binding proteins does NOT play a role in cell migration during chemotaxis? O Cap Z Rho Cdc42 O All of the listed GTPases play a role in cell migration O Rac ◆ Previous

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The phosphorylation of RNA polymerase II carboxyl-terminal domain is catalyzed by the protein kinase which is         .   options:   TFIIA   TFIIB   TFIIF   TFIIH

V- and t- tethering proteins SNARES GTPases NSFs mediate final docking between vesicle and target membranes. SNAPS

ATP and GTP play a few roles during transcription and translation. What are two roles that ATP plays and one role that GTP plays? GO S x2 x2 i T: B I

Match the protein on the left with the type of activation of that protein on the right STAT Smad PKA Ras NFKB Nuclear receptor [Choose] [Choose] GTP binding serine phosphorylation Interaction with Galpha Cleavage by y-secretase destruction of a protein by proteasome tyrosine phosphorylation second messenger ligand binding [Choose] [Choose] [Choose]

Can I get help on drawing a mechanism for the paragraph below? p53 stabilization by IR The signal upstream of p53 stabilization and activation after IR exposure most likely originate from DNA DSBs. This is supported by the fact that the kinases implicated in the phosphorylation of p53 are also implicated in DSB repair. These include two kinases that belong to the PI-3 kinase family, DNA-PK and ATM (see above), and indirectly, the checkpoint kinase 2 (Chk2). Ser15 of p53 was identified as a substrate for DNA-PK in vitro (Lees-Miller et al., 1992). Since DNA-PK is required for DSB repair in mammalian cells after IR exposure and since this residue falls within the MDM2-binding domain of the protein, this was an attractive model of p53 stabilization after IR. However, several recent reports have shown that Ser15 of p53 is phosphorylated in cells deficient in DNA-PK and that p53 accumulation in these cells is capable of generating cell cycle arrest or apoptosis after IR (Abraham et al.,…