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Human Polyclonal RNF8 Primary Antibody for IF, WB - ABIN522468
Morris, Boutell, Keppler, Densham, Weekes, Alamshah, Butler, Galanty, Pangon, Kiuchi, Ng, Solomon: The SUMO modification pathway is involved in the BRCA1 response to genotoxic stress. in Nature 2009
Show all 4 Pubmed References
deficiency of RNF8 sensitized breast cancer cells to combination of pharmacological inhibitors of Notch signaling and poly(ADP-ribose) polymerase (PARP), suggesting implications for treatment of breast cancer associated with impaired RNF8 expression or function.
Results reveal that RAD6B and RNF8 contribute to nucleosome removal during spermiogenesis.
Knockdown or conditional knockout of RNF8 or UBC13 in rodent cerebellar granule neurons robustly increases the number of parallel fiber presynaptic boutons and functional parallel fiber/Purkinje cell synapses. In contrast to the role of nuclear RNF8 in proliferating cells, RNF8 operates in the cytoplasm in neurons to suppress synapse differentiation.
RNF8-dependent polyubiquitination is required for the establishment of H3K27 acetylation, a marker of active enhancers, while persistent H2AK119ub inhibits establishment of H3K27 acetylation. Following the deposition of H3K27 acetylation, H3K4 dimethylation is established as an active mark on poised promoters.
RNF8-promoted Twist ubiquitination is required for Twist localization to the nucleus for subsequent epithelial-mesenchymal transition and cancer stem cells functions, thereby conferring chemoresistance.
Structure-guided separation-of-function mutations show that the RNF8 E2 stimulating activity is essential for DSB signaling in mammalian cells and is necessary for downstream recruitment of 53BP1 and BRCA1.
RNF8(-/-) mice exhibit neuronal degeneration and reactive astrocytosis. Neurons from RNF8(-/-) mice appear to be more susceptible to X-ray-induced DNA damage
Altogether, the data in this study highlight the importance of p53-pathway activation upon loss of Rnf8, suggesting that Rnf8 and p53 functionally interact to protect against genomic instability and tumorigenesis.
The identification of RNF8 allows new insights into the integration of the control of p12 degradation by different DNA damage signaling pathways.
RNF8-dependent ubiquitination of histone H2A during meiosis establishes active epigenetic modifications, including dimethylation of H3K4 on the sex chromosomes
A new mechanism of chromatin remodelling-assisted ubiquitylation was shown, which involves cooperation between CHD4 and RNF8 to create a local chromatin environment permissive to the assembly of checkpoint and repair machineries at DNA lesions.
Rnf8 physically interacts with Tpp1 to generate Ubc13-dependent Lys63 polyubiquitin chains that stabilize Tpp1 at telomeres.
RNF8 and Chfr, function together to activate ATM and maintain genomic stability in vivo.
53BP1 protein binds to Rnf8, suggesting DNA damage involves RNF8 dependent ubiquitylation, which allows its accumulation at damaged chromatin.
RNF8 deficint mice exhibit increased genomic instability and elevated risks for tumorigenesis indicating that Rnf8 is a novel tumor suppressor.
investigate the role of the ubiquitin ligase RNF8 during spermatogenesis and find that RNF8-deficient mice are proficient in meiotic sex chromosome inactivation but deficient in global nucleosome removal
subset of PTIP.PA1 complex is recruited to DNA damage sites via the RNF8-dependent pathway and is required for cell survival in response to DNA damage.
UV-induced NONO degradation by RNF8 is required for timely termination of intra-S-phase checkpoint signaling and continued cell cycle progression.
data are in line with a model in which HUWE1 primes histone H1 with ubiquitin to allow ubiquitin chain elongation by RNF8, thereby stimulating the RNF8-RNF168 mediated DDR.
L3MBTL2 orchestrates ubiquitin signalling by dictating the sequential recruitment of RNF8 and RNF168 after DNA damage, regulating the DNA damage response pathway.
study describes RNF8 as a co-activator of ERalpha increases ERalpha stability via post-transcriptional pathway, and provides a new insight into mechanisms for RNF8 to promote cell growth of ERalpha-positive breast cancer.
the present study described the noncovalent interaction between the E3 ubiquitin ligase RNF8 and SUMO2/3 and indicated that this interaction promoted DSB repair.
Data report that RNF8 is overexpressed in highly metastatic breast cell lines and its overexpression can induce EMT in breast cancer cells. Furthermore, RNF8 is aberrantly expressed in invasive breast cancer and positively correlates with lymph node metastasis.
The present findings indicate that WRAP53beta and RNF8 are rate-limiting factors in the repair of DNA double-strand breaks and raise the possibility that upregulation of WRAP53beta may contribute to genomic stability in and survival of cancer cells.
The study identifies a previously unrecognized role for RNF8 in the negative regulation of NF-kappaB activation by targeting and deactivating the IKK complex.
the role of RNF8-mediated histone H3 polyubiquitylation in the regulation of histone H3 stability and chromatin modification, is reported.
RNF8- and Ube2S-dependent Lys11-linkage ubiquitin conjugation plays an important role in regulating DNA damage-induced transcriptional silencing, distinct from the role of Lys63-linkage ubiquitin in the recruitment of DNA damage repair proteins 53BP1 and BRCA1.
The attenuated DNA damage localization of RNF8 resulting from INT6 depletion could be attributed to the defective retention of ATM.
In late S/G2 phase, the DNA damage-responsive E3 ligase RNF8 conjugates K63-linked ubiquitin chains to tankyrase 1, while in G1 phase such ubiquitin chains are removed by BRISC, an ABRO1/BRCC36-containing deubiquitinase complex.
Findings indicate direct interaction of dual-specificity tyrosine phosphorylation-regulated kinase 2 (DYRK2) with ring finger protein (C3HC4 type) 8 (RNF8) in regulating response to DNA damage.
High RNF8 expression is associated with bladder cancer.
The interaction of MDC1 with RNF8, but not with ATM requires WRAP53beta, suggesting that WRAP53beta facilitates the former interaction without altering phosphorylation of MDC1 by ATM.
These findings elucidate deeply and extensively the mechanism of RNF8/RNF168 and USP11 to maintain the proper status of ubiquitylation gammaH2AX to repair double strand breaks.
define a novel function for ATDC in the RNF8-mediated DNA damage response and implicate RNF8 binding as a key determinant of the radioprotective function of ATDC
Results indicate that RNF8 recruits and ubiquitinates many factors to repair DNA damage thereby conferring radioresistance to nasopharyngeal cancer cells.
Significantly restored tolerance of RAD18-/- and RNF8-/- cells to camptothecin and olaparib without affecting Rad51 focus formation.
The protein encoded by this gene contains a RING finger motif and an FHA domain. This protein has been shown to interact with several class II ubiquitin-conjugating enzymes (E2), including UBE2E1/UBCH6, UBE2E2, and UBE2E3, and may act as an ubiquitin ligase (E3) in the ubiquitination of certain nuclear proteins. This protein is also known to play a role in the DNA damage response and depletion of this protein causes cell growth inhibition and cell cycle arrest. Alternative splicing results in multiple transcript variants.
E3 ubiquitin-protein ligase RNF8
, ActA binding protein 2
, actA-interacting protein 37
, C3HC4-type zinc finger protein
, UBC13/UEV-interacting ring finger protein
, ring finger protein (C3HC4 type) 8
, E3 ubiquitin-protein ligase RNF8 A
, E3 ubiquitin-protein ligase RNF8-A
, RING finger protein 8 A
, RING finger protein 8-A