{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSCAP (the SREBP cleavage‐activating protein) is a conserved, multi‐transmembrane endoplasmic reticulum protein that functions as a sterol sensor and chaperone for SREBPs, the master transcription factors that drive lipid and cholesterol biosynthesis. Under low‐cholesterol conditions or oncogenic stimulation (for example, via EGFR signaling), SCAP undergoes N‐glycosylation and conformational changes that weaken its inhibitory binding to Insig proteins. This permits the SCAP–SREBP complex to exit the ER and transit to the Golgi where SREBPs are proteolytically activated to induce expression of lipogenic genes. Extensive structural and biochemical studies—including cryo–electron microscopy analyses of SCAP–Insig complexes—have provided detailed insights into how cholesterol binding to luminal loops (and associated COPII‐binding motifs) modulates SCAP trafficking and recycling, thereby establishing a central feedback mechanism in cholesterol homeostasis and metabolic regulation in liver, cancer cells, and in fatty liver disease contexts."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its canonical role in lipogenesis, SCAP is subject to extensive post‐translational regulation and engages in diverse protein–protein interactions that fine–tune its stability and signaling output. Interactions with E3 ubiquitin ligases—such as TRC8 and RNF5—mediate ubiquitination events that promote SCAP degradation or enhance its ability to foster conformational changes required for SREBP activation. Additional modulators including TMEM33 and GP73 have been shown to influence the lysosomal turnover of SCAP or strengthen its association with SREBPs. Moreover, by interacting with viral proteins (for example, in dengue virus and hepatitis B virus infection) and mediating inflammatory responses (such as in SARS‐CoV‐2 nucleocapsid–induced inflammasome activation), SCAP emerges as a central signaling hub that integrates metabolic cues with immune and stress signals. Genetic studies further link variants in SCAP (and its partner genes in the INSIG–SCAP–SREBP axis) to metabolic phenotypes such as dyslipidemia, altered blood pressure, drug–induced weight gain, and obesity. Collectively, these findings underscore SCAP’s pivotal role not only in maintaining cholesterol homeostasis but also in coordinating diverse cellular responses in health and disease."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Chunming Cheng, Peng Ru, Feng Geng, et al. 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