Dclre1c Activators
DCLRE1C, a key player in V(D)J recombination and DNA repair, exhibits single-strand-specific 5'-3' exonuclease and endonuclease activities on various DNA structures. Mutations in this gene can lead to severe combined immunodeficiency (SCID) and Omenn syndrome. Activation of DCLRE1C is crucial for its role in maintaining genomic integrity and responding to DNA damage. DCLRE1C is directly activated by genotoxic chemicals like camptothecin, etoposide, and bleomycin, inducing DNA damage and promoting its engagement in DNA repair and V(D)J recombination. Mitomycin C and cisplatin activate DCLRE1C by inducing DNA cross-links, highlighting its role in recognizing and processing diverse DNA lesions. Additionally, chemicals such as hydroxyurea and aphidicolin activate DCLRE1C by inducing replication stress, emphasizing its contribution to maintaining genomic stability during DNA replication challenges.
The general mechanisms of activation involve the recognition and processing of specific DNA structures generated by genotoxic stress. DCLRE1C acts as a guardian of genomic integrity, responding to challenges in DNA structure and replication. The diverse array of activators reflects the intricate regulatory network that ensures a robust and specific cellular response to different types of DNA damage. Understanding the activation mechanisms of DCLRE1C contributes to the knowledge of DNA repair processes and potential interventions for associated genetic disorders.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Camptothecin | 7689-03-4 | sc-200871 sc-200871A sc-200871B | 50 mg 250 mg 100 mg | $58.00 $186.00 $94.00 | 21 | |
Camptothecin, a topoisomerase I inhibitor, directly activates DCLRE1C by inducing DNA damage. This triggers the protein's involvement in DNA repair and V(D)J recombination. The activation of DCLRE1C by camptothecin is mediated through the recognition and processing of damaged DNA structures, highlighting its role in maintaining genomic integrity. | ||||||
Etoposide (VP-16) | 33419-42-0 | sc-3512B sc-3512 sc-3512A | 10 mg 100 mg 500 mg | $51.00 $231.00 $523.00 | 63 | |
Etoposide acts as a direct activator of DCLRE1C by inducing DNA damage and promoting the protein's involvement in DNA repair and V(D)J recombination. The activation occurs through the recognition and processing of DNA lesions, emphasizing the crucial role of DCLRE1C in maintaining genomic stability in response to cellular stress. | ||||||
Bleomycin | 11056-06-7 | sc-507293 | 5 mg | $275.00 | 5 | |
Bleomycin serves as a direct activator of DCLRE1C by causing DNA damage and triggering the protein's engagement in DNA repair and V(D)J recombination. The activation involves the recognition and processing of DNA lesions, underscoring the significance of DCLRE1C in safeguarding genomic integrity during cellular responses to genotoxic stress. | ||||||
Mitomycin C | 50-07-7 | sc-3514A sc-3514 sc-3514B | 2 mg 5 mg 10 mg | $66.00 $101.00 $143.00 | 85 | |
Mitomycin C directly activates DCLRE1C by inducing DNA cross-links, leading to the protein's engagement in DNA repair and V(D)J recombination. The activation involves the recognition and processing of cross-linked DNA structures, highlighting the crucial role of DCLRE1C in maintaining genomic stability during cellular responses to DNA damage. | ||||||
Cisplatin | 15663-27-1 | sc-200896 sc-200896A | 100 mg 500 mg | $138.00 $380.00 | 101 | |
Cisplatin acts as a direct activator of DCLRE1C by causing DNA damage, leading to the protein's involvement in DNA repair and V(D)J recombination. The activation occurs through the recognition and processing of DNA lesions, emphasizing the essential role of DCLRE1C in preserving genomic integrity during cellular responses to genotoxic stress. | ||||||
Hydroxyurea | 127-07-1 | sc-29061 sc-29061A | 5 g 25 g | $78.00 $260.00 | 18 | |
Hydroxyurea directly activates DCLRE1C by inducing replication stress, promoting the protein's engagement in DNA repair and V(D)J recombination. The activation involves the recognition and processing of DNA lesions, highlighting the crucial role of DCLRE1C in maintaining genomic stability during cellular responses to challenges in DNA replication. | ||||||
Fluorouracil | 51-21-8 | sc-29060 sc-29060A | 1 g 5 g | $37.00 $152.00 | 11 | |
Fluorouracil serves as a direct activator of DCLRE1C by causing DNA damage, leading to the protein's involvement in DNA repair and V(D)J recombination. The activation occurs through the recognition and processing of DNA lesions, emphasizing the essential role of DCLRE1C in preserving genomic integrity during cellular responses to genotoxic stress. | ||||||
Methyl methanesulfonate | 66-27-3 | sc-250376 sc-250376A | 5 g 25 g | $56.00 $133.00 | 2 | |
Methyl methanesulfonate (MMS) directly activates DCLRE1C by inducing DNA damage, triggering the protein's engagement in DNA repair and V(D)J recombination. The activation involves the recognition and processing of DNA lesions, underscoring the significance of DCLRE1C in maintaining genomic stability during cellular responses to genotoxic stress. | ||||||
Doxorubicin | 23214-92-8 | sc-280681 sc-280681A | 1 mg 5 mg | $176.00 $426.00 | 43 | |
Doxorubicin acts as a direct activator of DCLRE1C by causing DNA damage, leading to the protein's involvement in DNA repair and V(D)J recombination. The activation occurs through the recognition and processing of DNA lesions, emphasizing the essential role of DCLRE1C in preserving genomic integrity during cellular responses to genotoxic stress. | ||||||
Aphidicolin | 38966-21-1 | sc-201535 sc-201535A sc-201535B | 1 mg 5 mg 25 mg | $84.00 $306.00 $1104.00 | 30 | |
Aphidicolin directly activates DCLRE1C by inducing replication stress, promoting the protein's engagement in DNA repair and V(D)J recombination. The activation involves the recognition and processing of DNA lesions, highlighting the crucial role of DCLRE1C in maintaining genomic stability during cellular responses to challenges in DNA replication. | ||||||