Rabbit Polyclonal TREX1 antibody. Suitable for IP, IHC-P and reacts with Human samples. Immunogen corresponding to Recombinant Fragment Protein within Human TREX1 aa 1-300.
pH: 7.3
Preservative: 0.02% Sodium azide
Constituents: PBS, 50% Glycerol (glycerin, glycerine)
IP | IHC-P | |
---|---|---|
Human | Tested | Tested |
Species | Dilution info | Notes |
---|---|---|
Species Human | Dilution info 1/200.00000 - 1/2000.00000 | Notes - |
Species | Dilution info | Notes |
---|---|---|
Species Human | Dilution info 1/20.00000 - 1/200.00000 | Notes - |
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Major cellular 3'-to-5' DNA exonuclease which digests single-stranded DNA (ssDNA) and double-stranded DNA (dsDNA) with mismatched 3' termini (PubMed:10391904, PubMed:10393201, PubMed:17293595). Prevents cell-intrinsic initiation of autoimmunity (PubMed:10391904, PubMed:10393201, PubMed:17293595). Acts by metabolizing DNA fragments from endogenous retroelements, including L1, LTR and SINE elements (PubMed:10391904, PubMed:10393201, PubMed:17293595). Plays a key role in degradation of DNA fragments at cytosolic micronuclei arising from genome instability: its association with the endoplasmic reticulum membrane directs TREX1 to ruptured micronuclei, leading to micronuclear DNA degradation (PubMed:33476576). Micronuclear DNA degradation is required to limit CGAS activation and subsequent inflammation (PubMed:33476576). Unless degraded, these DNA fragments accumulate in the cytosol and activate the cGAS-STING innate immune signaling, leading to the production of type I interferon (PubMed:33476576). Prevents chronic ATM-dependent checkpoint activation, by processing ssDNA polynucleotide species arising from the processing of aberrant DNA replication intermediates (PubMed:18045533). Inefficiently degrades oxidized DNA, such as that generated upon antimicrobial reactive oxygen production or upon absorption of UV light (PubMed:23993650). During GZMA-mediated cell death, contributes to DNA damage in concert with NME1 (PubMed:16818237). NME1 nicks one strand of DNA and TREX1 removes bases from the free 3' end to enhance DNA damage and prevent DNA end reannealing and rapid repair (PubMed:16818237).
Three-prime repair exonuclease 1, 3'-5' exonuclease TREX1, Deoxyribonuclease III, DNase III, TREX1
Rabbit Polyclonal TREX1 antibody. Suitable for IP, IHC-P and reacts with Human samples. Immunogen corresponding to Recombinant Fragment Protein within Human TREX1 aa 1-300.
pH: 7.3
Preservative: 0.02% Sodium azide
Constituents: PBS, 50% Glycerol (glycerin, glycerine)
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TREX1 also known as Three Prime Repair Exonuclease 1 acts as a DNA exonuclease which degrades single-stranded DNA from the 3' end. This protein exhibits a mass of 33 kDa. TREX1's expression is largely found in the cytoplasm of many cell types including those in the immune system and various tissues like the liver spleen and heart. Through its enzymatic activity TREX1 helps maintain genomic stability by processing DNA intermediates that arise from incomplete DNA replication or repair processes.
TREX1 removes excessive DNA that might trigger immune responses. It is not a part of a large protein complex but works closely with substrates involved in DNA repair and replication. By degrading abnormal DNA TREX1 prevents the initiation of inappropriate immune responses that could result in autoimmunity. Its functionality is essential in preventing the cell from converting these DNA fragments into ligands for DNA sensors which could activate immune signaling pathways.
TREX1 plays a significant role in the DNA damage response and innate immune pathways. In the DNA damage response pathway TREX1 functions alongside proteins like ATR and ATM which address DNA replication stress and repair. Within the innate immune pathway it interacts with cGAS (cyclic GMP-AMP synthase) which can become activated in response to cytosolic DNA leading to the production of type I interferons - powerful immune modulators.
Mutations in TREX1 have been linked to autoimmune diseases such as Aicardi-Goutières syndrome and systemic lupus erythematosus. In these conditions the altered or deficient TREX1 leads to the accumulation of DNA in the cytoplasm falsely triggering an antiviral immune response. This relationship with cGAS is critical as the cGAS-STING pathway becomes activated due to the presence of unprocessed DNA resulting in chronic inflammation and contributing to the autoimmune pathology observed in these disorders.
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Paraffin-embedded human small intestine tissue stained for TREX1 using ab238339 at 1/100 dilution in immunohistochemical analysis.
TREX1 was immunoprecipitated from 0.5 mg HeLa (Human epithelial cell line from cervix adenocarcinoma) whole cell extract with ab238339 at 1/200 dilution.
Lane 1: Control rabbit IgG IP (1 μg) in HeLa whole cell lysate.
Lane 2: ab238339 IP in HeLa whole cell lysate.
Lane 3: HeLa whole cell lysate 20 μg (Input).
For Western blotting, an HRP-conjugated anti-rabbit IgG, specific to the non-reduced form of IgG was used as the secondary antibody at 1/50,000 dilution.
All lanes: Immunoprecipitation - Anti-TREX1 antibody (ab238339)
Predicted band size: 39 kDa
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