EME1 antibodies are immunological reagents designed to bind specifically to the EME1 protein, enabling its detection and quantification in experimental settings. EME1 forms a heterodimeric complex with MUS81, functioning as a structure-specific endonuclease critical for resolving DNA replication intermediates and repairing double-strand breaks . These antibodies are widely used in Western blot (WB), immunofluorescence (IF), and immunohistochemistry (IHC) to investigate EME1's role in cancer biology, genomic stability, and therapeutic resistance .
Gastric Cancer (GC): EME1 is overexpressed in GC tissues and cell lines (e.g., AGS, MGC-803). Knockdown studies using siRNA and EME1 antibodies revealed its role in promoting proliferation, migration, and invasion via the Akt/GSK3B/CCND1 pathway. Silencing EME1 reduced tumor growth in xenograft models .
PARP Inhibitor (PARPi) Resistance: In BRCA1/ATM-deficient cancers, EME1 downregulation restores homologous recombination (HR) capacity, driving PARPi resistance. SETD1A-mediated EME1 transcription correlates with PARPi sensitivity, highlighting EME1 as a biomarker for therapy response .
Nucleolar Localization: EME1 accumulates in nucleolar repair condensates after camptothecin (CPT)-induced DNA damage. Sumoylation regulates its nuclear-cytoplasmic shuttling, with poly-sumoylated EME1 variants showing distinct localization patterns .
Genomic Stability: Eme1–/– embryonic stem cells exhibit hypersensitivity to DNA cross-linking agents (e.g., mitomycin C) and spontaneous genomic instability, underscoring EME1's role in interstrand cross-link repair .
Specificity: Validation via RNAi or CRISPR knockout is critical, as off-target signals are common. For example, Santa Cruz’s MTA31 7h2/1 clone shows robust specificity in WB .
Subcellular Localization: EME1 is predominantly cytoplasmic under unstressed conditions but translocates to nuclei upon DNA damage. Antibodies like Coring System’s polyclonal serum are optimal for IF-based localization studies .
High EME1 expression correlates with poor prognosis in gastric, pancreatic, and esophageal cancers . Therapeutic targeting of EME1 or its interactors (e.g., Akt) may enhance chemosensitivity. For instance, EME1 knockdown synergizes with PARPi in HR-deficient models .
KEGG: ago:AGOS_ADL318C
STRING: 33169.AAS51602