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Validated All-in-One™ qPCR Primer for MRE11(NM_005591.3) Search again
Product ID:
HQP011321
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ATLD, HNGS1, MRE11A, MRE11B
Gene Description:
MRE11 homolog, double strand break repair nuclease
Target Gene Accession:
NM_005591.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
This gene encodes a nuclear protein involved in homologous recombination, telomere length maintenance, and DNA double-strand break repair. By itself, the protein has 3' to 5' exonuclease activity and endonuclease activity. The protein forms a complex with the RAD50 homolog; this complex is required for nonhomologous joining of DNA ends and possesses increased single-stranded DNA endonuclease and 3' to 5' exonuclease activities. In conjunction with a DNA ligase, this protein promotes the joining of noncomplementary ends in vitro using short homologies near the ends of the DNA fragments. This gene has a pseudogene on chromosome 3.
Gene References into function
- Major target for inactivation in mismatch repair-defective cells and may contribute to the development of colorectal cancer.
- Adenovirus oncoproteins inactivate the Mre11-Rad50-NBS1 DNA repair complex
- activation in response to replication-dependent DNA double-strand breaks induced by mammalian DNA topoisomerase I cleavage complexes
- Mre11 complex is required for both ATM activation and the ATM-dependent G(2)/M checkpoint in response to double stranded breaks.
- WRN associates with the Mre11 complex via binding to Nbs1 in vitro and in vivo.
- Functional and structural characterization of a nuclease-deficient Mre11 protein termed mre11-3.
- MRE11 is a new common target in the mismatch repair deficient tumorigenesis and has a role in colorectal carcinogenesis
- Replication protein A, Mre11, Rad50 and Nbs1 bind and have roles in DNA repair
- Two hours at 41 degrees C did not increase the radiation sensitivity of cells with a reduced Mre11 protein level following a 24-h siRNA treatment.
- Nibrin, Mre11 and Rad50 also act as adaptors for some downstream Atm phosphorylation events
- MRE11 gene mutations affected ATM-dependent responses in radiosensitive ataxia-telangiectasia-like disorder family.
- MRE11 expression is impaired in gastric cancer with microsatellite instability
- Data show that Mre11 complex proteins are present in neurons of the adult human cortex and cerebellum, and suggest that loss of the complex may be associated with the pathogenesis of Alzheimer disease.
- early-onset, slowly progressive, ataxia plus ocular apraxia phenotype = ataxia telangiectasia-like disorder (ATLD)
- the Mre11/Rad50/Nbs1 (MRN) complex may play a more universal role in the recognition and response to DNA lesions of all types, whereas the role of RPA may be limited to certain subsets of lesions
- findings show that the Mre11-Rad50-Nbs1 (MRN) complex acts as a double-strand break sensor for ATM and recruits ATM to broken DNA molecules
- hMRE11 represents a functional component of the DNA mismatch repair pathway
- The MRE11-RAD50-NBS1 complex accelerates somatic hypermutation and gene conversion of immunoglobulin variable regions.
- These results suggest that MRE11 methylation regulates its association with nuclear structures such as PML nuclear bodies and sites of DNA damage.
- the dynamic architecture of human Rad50/Mre11/Nbs1 is markedly affected by DNA binding
- Adenovirus 5 exploits the cellular aggresome response to accelerate inactivation of MRE11-RAD50-NBS1 (MRN) complexes that otherwise inhibit viral DNA replication and packaging.
- We show that Mre11 are required for the processing of DNA double-strand breaks (DSBs) to generate the replication protein A (RPA)-coated ssDNA that is needed for ATR recruitment and the subsequent phosphorylation and activation of Chk1.
- the data are not compatible with selective pressures during tumorigenesis promoting the functional loss of BRCA2 and MRE11 in microsatellite unstable tumors, but fit closely with an absence of selective pressures acting on BRCA2 and MRE11 gene status
- ATM and Mre11 may stimulate the ATR signaling pathway by converting DNA damage generated by ionizing radiation into structures that recruit and activate ATR
- the Mre11-Rad50-Nbs1 complex stayed in the nucleus and remained intact in response to hypertonicity
- Mre11 stabilizes Nbs1 and Rad50 and MRN activates Chk2 downstream from ATM in response to replication-mediated DNA double strand breaks
- Part played by Mre11 in telomere maintenance may not be important for the progression of lung adenoma-carcinoma although some role for it in carcinogenesis cannot be completely ruled out.
- MRE11, but not RAD50 or NBS1 variants, may play a role in non-Hodgkin's lymphoma
- maintenance of higher expression of Ku70 and Mre11 may be responsible for keeping longer life span observed in the longevity group
- Mre11/Rad50 complexes from three organisms catalyze the reversible adenylate kinase reaction in vitro.
- The results are consistent with a model in which Mre11 interferes with DNA replication when it is localized at viral DNA replication foci.
- the Mre11-Rad50-Nbs1 complex plays critical roles both upstream and downstream of ATR to regulate the S-phase checkpoint when replication forks are stalled
- microsatelite instability and alterations in the MRE11 and RAD50 repeats that are associated with the reduced protein expression and functional impairment of the MRE11-RAD50-NBS1 complex in Lynch syndrome
- Data demonstrate that Mre11/Rad50/Nbs1 interacts with replication protein A in unperturbed cells, that the interaction is regulated by cyclin-dependent kinases, and that this interaction is needed for MRN to correctly localize to replication centers.
- the MRN (MRE11/RAD50/NBS1)complex, and especially NBS1, is required for alternative lengthening of telomeres
- TRF1 association with telomeres induced by ATM inhibition is abrogated in cells lacking MRE11 or NBS1, suggesting that MRN and ATM function in the same pathway controlling TRF1 binding to telomeres
- These data support a role for RPA as an initial signal/sensor for DNA damage that facilitates recruitment of MRE11/RAD50/NBS1 and ATM/ATR to sites of damage, where they then work together to fully activate the DNA damage response.
- Studies suggest new roles of Mre11/Rad50/Nbs1 complex in the maintenance of genome stability through preventing rereplication and rereplication-associated double-stranded breaks when licensing control is compromised.
- Mre11/Rad50/Nbs1 complex (MRN) poses a barrier to adeno-associated virus and that the helper function provided by E1b55K/E4orf6 involves MRN degradation.
- Hypothesis examined in a study of 559 breast cancer patients of single-nucleotide polymorphisms in Mre11, Rad50, and Nbs1 and by the in vivo detection of binding between Mre11 and BRCA1, encoded by the breast cancer susceptibility gene BRCA1.
- Rapid accumulation of MRE11 and NBS1 at sites of DNA damage requires PARP1.
- NBS1 and MRE11 promote replication-associated recombination junctions essential for EBV episomal maintenance and genome stability
- These results suggest that Mre11 loss following HSV-1 infection is caused by the generation of free DNA ends during or following viral DNA replication.
- Results are consistent with a model in which physical interaction of Mre11 with viral DNA is mediated by Nbs1, and interferes with viral DNA replication.
- a mutant allele of MRE11 found in a colon cancer cell line sensitizes cells to agents causing replication fork stress. The mutant Mre11 weakly interacts with Rad50 relative to wild type and shows little affinity for Nbs1.
- GAR domain plays an important role in regulating MRE11 function at the biochemical and cellular levels during DNA double-strand break repair.
- Analysis of 38 hMLH1 missense mutations showed that the majority of mutations caused significant (>50%) reductions in their interaction with hMRE11.
- Snm1B interacts with the Mre11-Rad50-Nbs1 (MRN) complex and with FancD2 further substantiating its role as a checkpoint/DNA repair protein.
- These results suggest that Mre11-Rad50-Nbs1-dependent generation of ssDNA oligos, which constitute a unique signal of ongoing double-strand breaks repair not encountered in normal DNA metabolism, stimulates ATM activity.
- Transcription-coupled DNA double-strand breaks are mediated via the nucleotide excision repair and the Mre11-Rad50-Nbs1 complex
- Assessment of carriers' frequency of a novel MRE11A mutation responsible for the rare ataxia telangiectasia-like disorder is presented.
- ATM, Mre11, and Rad50 are required for survival after replication fork stalling.
- RAD50/MRE11/NBS1 proteins interacted with each other, which had different clinicopathological significance in microsatellite-stable and -unstable colorectal cancer