Rif1 Inhibitors
Replication timing regulatory factor 1 (Rif1) is a pivotal protein involved in the regulation of DNA replication timing, telomere length maintenance, and genomic stability. It plays a crucial role in ensuring the proper spatial and temporal coordination of DNA replication, acting as a guardian of the genome's integrity by influencing the replication timing program across various cell types and developmental stages. Rif1 exerts its regulatory function through the recruitment of protein complexes to replication origins, thereby modulating the initiation and progression of DNA synthesis. This protein is also integral to the repair of double-strand breaks (DSBs), a critical aspect of cellular defense mechanisms against genomic instability. By controlling the access of repair machinery to broken DNA ends, Rif1 significantly influences the choice of repair pathway, favoring non-homologous end joining (NHEJ) over homologous recombination (HR), a process vital for maintaining genomic stability and disrupting deleterious rearrangements.
The inhibition of Rif1 involves mechanisms that directly impact its ability to perform its regulatory functions, affecting DNA replication timing, telomere length management, and genomic stability. Inhibitory processes may target the protein's interaction domains, blocking its association with DNA or other proteins essential for its function. Such inhibition can lead to alterations in the replication timing across the genome, causing asynchronous replication initiation, replication stress, and an increased risk of genomic instability. Additionally, inhibiting Rif1's function in DSB repair pathway choice can lead to a shift in the balance between NHEJ and HR, affecting the efficiency and fidelity of DNA repair processes. This disruption in Rif1's activities highlights its critical role in maintaining cellular homeostasis and genomic integrity. Through these mechanisms, the inhibition of Rif1 directly affects cellular processes fundamental to the preservation of genomic information and the disruption of genomic aberrations, underlining the protein's importance in cellular biology and genomic regulation.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
ATM Kinase Inhibitor | 587871-26-9 | sc-202963 | 2 mg | $108.00 | 28 | |
ATM Kinase Inhibitor directly influences DNA damage response pathways. ATM activation is crucial for Rif1 phosphorylation and subsequent localization to DNA damage sites. By inhibiting ATM, KU-55933 reduces Rif1 phosphorylation and impairs its recruitment to DNA double-strand breaks, thereby indirectly modulating Rif1's role in DNA repair. | ||||||
ATM/ATR Kinase Inhibitor Inhibitor | 905973-89-9 | sc-202964 | 5 mg | $104.00 | 8 | |
ATM/ATR Kinase Inhibitor affects Rif1 indirectly by targeting these kinases. Since Rif1 is a downstream effector of ATM/ATR-mediated signaling in response to DNA damage, inhibiting these kinases with CGK733 decreases Rif1's activation and its subsequent cellular functions in DNA repair and replication timing regulation. | ||||||
NU 7441 | 503468-95-9 | sc-208107 | 5 mg | $350.00 | 10 | |
A potent inhibitor of DNA-dependent protein kinase (DNA-PK), NU7441 indirectly influences Rif1 by affecting the DNA damage response. Rif1 is involved in DNA repair processes regulated by DNA-PK. By inhibiting DNA-PK, NU7441 can decrease Rif1's recruitment and functionality at DNA damage sites, thereby modulating its role in DNA repair mechanisms. | ||||||
VE 821 | 1232410-49-9 | sc-475878 | 10 mg | $360.00 | ||
VE-821, an ATR inhibitor, indirectly modulates Rif1 activity. ATR kinase is involved in the activation of downstream proteins like Rif1 in response to replication stress. By inhibiting ATR, VE-821 reduces Rif1 phosphorylation and disrupts its function in the DNA damage response and replication timing control. | ||||||
MRN-ATM Pathway Inhibitor, Mirin | 299953-00-7 | sc-203144 | 10 mg | $138.00 | 4 | |
Mirin, an inhibitor of the Mre11-Rad50-Nbs1 (MRN) complex, indirectly affects Rif1. The MRN complex is essential for the recruitment and activation of ATM, a kinase that phosphorylates Rif1. By inhibiting the MRN complex, Mirin reduces ATM activation and consequently decreases Rif1 phosphorylation, impacting its role in DNA repair. | ||||||
BML-277 | 516480-79-8 | sc-200700 sc-200700A | 10 mg 50 mg | $129.00 $482.00 | 2 | |
CHK1 inhibitors target CHK1 kinase, which is involved in cell cycle control and the DNA damage response. CHK1 modulates Rif1's activity in replication timing and DNA repair. By inhibiting CHK1, these compounds can disrupt Rif1-mediated processes in response to DNA damage and replication stress. | ||||||
Nutlin-3 | 548472-68-0 | sc-45061 sc-45061A sc-45061B | 1 mg 5 mg 25 mg | $56.00 $212.00 $764.00 | 24 | |
MDM2 inhibitors indirectly modulate Rif1 by stabilizing p53, a key regulator of the DNA damage response. p53 activation can influence Rif1's role in DNA repair and replication timing. By inhibiting MDM2, these compounds enhance p53 activity, which in turn can affect Rif1 function. | ||||||
ABT-888 | 912445-05-7 | sc-202901 sc-202901A sc-202901B | 1 mg 5 mg 25 mg | $115.00 $170.00 $500.00 | 24 | |
PARP inhibitors, by inhibiting poly(ADP-ribose) polymerase, can indirectly influence Rif1. PARP is involved in the repair of single-strand DNA breaks. Its inhibition can lead to the accumulation of DNA damage and the activation of pathways involving Rif1, thereby modulating its activity in DNA repair. | ||||||
BIX 02189 | 1094614-85-3 | sc-364436 sc-364436A | 5 mg 10 mg | $220.00 $378.00 | 5 | |
ATRX inhibitors indirectly modulate Rif1 by targeting the ATRX protein, involved in chromatin remodeling and DNA repair. Since Rif1 is associated with chromatin structure and DNA repair processes, inhibiting ATRX can impact Rif1's functionality in these contexts. | ||||||
CCT 018159 | 171009-07-7 | sc-202526 | 5 mg | $91.00 | ||
HSP90 inhibitors can indirectly affect Rif1 by destabilizing client proteins involved in the DNA damage response and replication stress pathways. Since Rif1 is a part of these pathways, inhibiting HSP90 can modulate Rif1's activity in DNA repair and replication timing control. | ||||||