Rad9 Activators
Rad9, a crucial component of the DNA damage response (DDR) pathway, functions as a sensor and mediator of the cell's response to DNA damage. By forming part of the 9-1-1 (Rad9-Rad1-Hus1) complex, Rad9 is integral to the activation of checkpoint signaling pathways that ensure the maintenance of genomic integrity. This complex is rapidly recruited to sites of DNA damage, where it serves to halt cell cycle progression and facilitate the repair of damaged DNA. Rad9's role extends beyond mere recruitment to damage sites; it is also involved in the amplification of DDR signals, enabling the sustained activation of repair mechanisms. This is achieved through its interaction with key DDR proteins, including ATR (ataxia-telangiectasia and Rad3-related protein), which phosphorylates a variety of substrates involved in cell cycle arrest, DNA repair, and apoptosis. The ability of Rad9 to coordinate these processes is vital for preventing the accumulation of genetic mutations and the onset of cancerous growths, highlighting its role as a guardian of genomic stability.
The activation of Rad9 within the DDR pathway involves a series of tightly regulated steps, beginning with its recruitment to DNA damage sites. This recruitment is facilitated by the recognition of DNA lesions or replication stress signals, often mediated by post-translational modifications such as phosphorylation. Phosphorylation of Rad9, for instance, enhances its ability to interact with other proteins and to stimulate its function within the 9-1-1 complex. Furthermore, the interaction of Rad9 with chromatin and other DDR proteins is modulated by its oligomerization state, which is influenced by specific DNA structures and the presence of other DDR factors. The activation of Rad9 is thus a complex process that involves changes in its post-translational modification status, alterations in its interaction partners, and its localization to sites of DNA damage. These mechanisms ensure that Rad9 is precisely activated in response to genotoxic stress, enabling the effective coordination of DNA repair and cell cycle arrest processes necessary for the preservation of cell viability and the prevention of disease.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Bleomycin | 11056-06-7 | sc-507293 | 5 mg | $275.00 | 5 | |
Bleomycin activates Rad9 by inducing DNA damage. The chemical induces double-strand breaks in DNA, leading to the activation of the DNA damage response (DDR) pathway, where Rad9 plays a crucial role in sensing and repairing damaged DNA. | ||||||
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 activates Rad9 by inhibiting topoisomerase II and inducing DNA damage. The resulting DNA breaks activate the DDR pathway, with Rad9 playing a key role in the recognition of damaged DNA and the initiation of repair processes. | ||||||
Hydroxyurea | 127-07-1 | sc-29061 sc-29061A | 5 g 25 g | $78.00 $260.00 | 18 | |
Hydroxyurea indirectly activates Rad9 by causing replication stress. It inhibits ribonucleotide reductase, leading to nucleotide pool depletion and replication fork stalling. Rad9 is subsequently recruited to stalled forks, activating the DDR pathway and promoting DNA repair. | ||||||
Camptothecin | 7689-03-4 | sc-200871 sc-200871A sc-200871B | 50 mg 250 mg 100 mg | $58.00 $186.00 $94.00 | 21 | |
Camptothecin activates Rad9 by inhibiting topoisomerase I, inducing DNA damage. This triggers the DDR pathway, where Rad9 functions in the recognition of DNA lesions and the initiation of repair processes, highlighting its role in maintaining genomic stability. | ||||||
Aphidicolin | 38966-21-1 | sc-201535 sc-201535A sc-201535B | 1 mg 5 mg 25 mg | $84.00 $306.00 $1104.00 | 30 | |
Aphidicolin activates Rad9 by causing replication stress. It inhibits DNA polymerase alpha and induces fork stalling, leading to the activation of the DDR pathway. Rad9 is involved in recognizing stalled forks and facilitating the repair of DNA damage induced by replication stress. | ||||||
Phleomycin | 11006-33-0 | sc-204845 sc-204845A | 5 mg 25 mg | $195.00 $495.00 | ||
Phleomycin activates Rad9 through its DNA-damaging properties. The chemical induces double-strand breaks, activating the DDR pathway, where Rad9 participates in sensing DNA damage and orchestrating the cellular response to maintain genomic integrity. | ||||||
Methyl methanesulfonate | 66-27-3 | sc-250376 sc-250376A | 5 g 25 g | $56.00 $133.00 | 2 | |
Methyl methanesulfonate activates Rad9 by alkylating DNA and inducing DNA damage. This triggers the DDR pathway, with Rad9 playing a critical role in recognizing and initiating the repair of DNA lesions caused by alkylation. | ||||||
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 activates Rad9 by forming DNA crosslinks and inducing DNA damage. This activates the DDR pathway, where Rad9 participates in the detection and repair of DNA lesions. The chemical's ability to induce DNA damage highlights Rad9's role in maintaining genomic stability. | ||||||
Fluorouracil | 51-21-8 | sc-29060 sc-29060A | 1 g 5 g | $37.00 $152.00 | 11 | |
Fluorouracil indirectly activates Rad9 by causing replication stress. The chemical is incorporated into DNA, leading to replication fork stalling and the activation of the DDR pathway. Rad9 is involved in recognizing stalled forks and facilitating DNA repair processes. | ||||||
2′-Deoxy-2′,2′-difluorocytidine | 95058-81-4 | sc-275523 sc-275523A | 1 g 5 g | $56.00 $128.00 | ||
2'-Deoxy-2',2'-difluorocytidine activates Rad9 by incorporating into DNA and inducing replication stress. The resulting stalled replication forks activate the DDR pathway, where Rad9 is crucial in recognizing and repairing DNA damage induced by the incorporation of gemcitabine during DNA synthesis. | ||||||