Insufficient information available to write a comprehensive gene function summary for GEM (GTP binding protein overexpressed in skeletal muscle). The provided PubMed abstracts focus exclusively on gemcitabine (GEM) chemotherapy resistance in pancreatic cancer and bladder cancer, discussing mechanisms involving unrelated proteins (RUNX1, circFARP1, hsa_circ_0007919, DLGAP5, TRIM29, HIF1A-AS1, and GAS41). One abstract discusses a genome-scale metabolic model framework also using the acronym 'GEM,' but contains no information about the GEM gene. None of the abstracts address the GTP-binding protein GEM, its molecular function, mechanism of action, disease associations, or clinical significance. To provide an accurate summary grounded in the provided sources, peer-reviewed literature specifically investigating GEM (GTPase) function, regulation, protein interactions, tissue-specific expression patterns, or disease relevance would be required. Based solely on UniProt and GO annotations without supporting abstracts, we cannot make evidence-based claims about this protein's specific roles in signal transduction, receptor regulation, or cell cycle processes.