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Target intelligence / Profile preview
Single-strand DNA endonuclease ASTE1 (ASTE1)
- Target
- ASTE1
- Molecular classification
- Enzyme, Endonuclease, DNA-binding protein
01
Overview
Single-strand DNA endonuclease ASTE1 is a structure-specific DNA endonuclease that cleaves single-stranded DNA and 3' overhang DNA, playing a crucial role in directing DNA double-strand break repair pathway choice[1][4][5][10]. ASTE1 acts downstream of the shieldin complex within the 53BP1-RIF1 DNA repair axis, promoting non-homologous end-joining (NHEJ) by cleaving single-stranded DNA ends and thus antagonizing BRCA1-dependent homologous recombination[1][2][3]. Recruited to DNA damage sites in a shieldin-dependent manner, loss of ASTE1 impairs NHEJ, leads to hyper-resection, defects in immunoglobulin class switching, and resistance to PARP inhibitors in BRCA1-deficient cells[1][3][5][10]. It is encoded by the ASTE1 gene (also known as asteroid homolog 1 or HT001) in humans.
- Other names
- Asteroid homolog 1HT001Protein asteroid homolog 1single-strand DNA endonuclease ASTE1asteroid homolog 1
02
Mechanism of action
Modulation of DNA repair pathway choice (antagonizing BRCA1-mediated homologous recombination, promoting NHEJ)[1][3][5]
03
Biological functions
DNA double-strand break repairNon-homologous end-joining (NHEJ)Regulation of homologous recombinationDNA damage responseImmunoglobulin class switch recombination
04
Disease associations
Cancer (notably via mechanism involving DNA repair, BRCA1-deficiency, and possible involvement in mismatch repair cancer syndromes)Mismatch repair cancer syndromeLynch syndrome
05
Safety considerations
Potential for genomic instability if targeted or impaired (due to defects in DSB repair)[1][3]Risk of cancer therapy resistance (if drug targeting results in loss of ASTE1 function in certain cancers)[1][3]
06
Interacting drugs
Poly(ADP-ribose) polymerase (PARP) inhibitors (drug resistance reported in BRCA1-deficient contexts due to ASTE1 loss)[1][3][5]
07
Biomarkers
ASTE1 deficiency (potential biomarker for PARP inhibitor resistance in BRCA1-deficient cancers)[1][3]
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