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#prenylation

2 public questions tagged with this topic.

The prenylation reaction occurs at which region of the protein?

Protein prenylation attaches hydrophobic isoprenoid to facilitate membrane association and protein-protein interactions. Substrate determinant is C-terminal CAAX box where C is cysteine acceptor, A aliphatic amino acids isoleucine, leucine, valine, X residue determining enzyme specificity methionine, serine, glutamine for farnesyltransferase versus leucine for geranylgeranyltransferase I, while Rab proteins contain CC, CXC motifs recognized by geranylgeranyltransferase II. Reaction catalyzed by cytosolic heterodimeric transferases FTase, GGTase I, GGTase II using farnesyl or geranylgeranyl pyrophosphate, forming thioether linkage to cysteine sulfur at extreme carboxyl terminus. After prenylation, endoplasmic reticulum enzymes RCE1 protease removes AAX tripeptide and ICMT methyltransferase methylates newly exposed carboxyl enhancing hydrophobicity. Therefore prenylation occurs at C-terminal cysteine, not N-terminal glycine characteristic of myristoylation nor internal serine which undergoes O-phosphorylation or O-GlcNAcylation. This C-terminal lipidation positions Ras, Rho, Rab, lamins at appropriate membranes including plasma membrane, endosome and nuclear envelope for functional signaling. Such detailed mechanistic insight is frequently examined in competitive tests including NEET, CUET, CSIR-NET and GATE where transporter classification, energetics and disease linkage are integrated into problem-solving questions.

Ref: Zhang & Casey, Annu Rev Biochem 1996, CAAX prenylation; Wang & Casey, Nat Rev Mol Cell Biol 2016.

Which lipid anchor type is involved in signal transduction and is found in Ras protein?

Ras small GTPases H-Ras, N-Ras, K-Ras are central hubs in growth factor signaling linking receptor tyrosine kinases to Raf-MEK-ERK MAPK cascade regulating proliferation, differentiation, survival and cytoskeletal remodeling. For signaling competence Ras must associate with inner leaflet of plasma membrane where it interacts with effectors. This localization depends on C-terminal CAAX prenylation. H-Ras, N-Ras, K-Ras4A undergo farnesylation of CAAX cysteine by farnesyltransferase forming thioether linked 15-carbon anchor, followed by RCE1 cleavage and ICMT methylation. Additional second signal provided by palmitoylation of upstream cysteines for H-Ras and N-Ras or polybasic stretch for K-Ras4B enhances stable membrane binding and partitioning to distinct microdomains. GPI anchoring attaches extracellularly and myristoylation occurs at N-terminal glycine, not relevant to Ras, which is prenylated C-terminally. Oncogenic mutations lock Ras GTP-bound active causing constitutive signaling, making membrane association via farnesylation crucial therapeutic target for inhibitor development in cancer biology. Such detailed mechanistic insight is frequently examined in competitive tests including NEET, CUET, CSIR-NET and GATE where transporter classification, energetics and disease linkage are integrated into problem-solving questions.

Ref: Hancock, Nat Rev Mol Cell Biol 2003, Ras membrane targeting; Prior et al., Cancer Res 2012.