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Mouse Anti-PARN Recombinant Antibody (CBYC-P171) (CBMAB-P0800-YC)

Provided herein is a Mouse monoclonal antibody against Human Poly(A)-Specific Ribonuclease. The antibody can be used for immunoassay techniques, such as ICC, WB.
See all PARN antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBYC-P171
Antibody Isotype
IgM, κ
Application
ICC, WB

Basic Information

Specificity
Human
Antibody Isotype
IgM, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
PBS, pH 7.2
Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at-20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
poly(A)-specific ribonuclease
Introduction
PARN is a 3'-exoribonuclease, with similarity to the RNase D family of 3'-exonucleases. It prefers poly(A) as the substrate, hence, efficiently degrades poly(A) tails of mRNAs. Exonucleolytic degradation of the poly(A) tail is often the first step in the decay of eukaryotic mRNAs. This protein is also involved in silencing of certain maternal mRNAs during oocyte maturation and early embryonic development, as well as in nonsense-mediated decay (NMD) of mRNAs that contain premature stop codons.
Entrez Gene ID
UniProt ID
Alternative Names
Poly(A)-Specific Ribonuclease; Deadenylation Nuclease; Polyadenylate-Specific Ribonuclease; Deadenylating Nuclease; EC 3.1.13.4; DAN;
Function
3'-exoribonuclease that has a preference for poly(A) tails of mRNAs, thereby efficiently degrading poly(A) tails. Exonucleolytic degradation of the poly(A) tail is often the first step in the decay of eukaryotic mRNAs and is also used to silence certain maternal mRNAs translationally during oocyte maturation and early embryonic development. Interacts with both the 3'-end poly(A) tail and the 5'-end cap structure during degradation, the interaction with the cap structure being required for an efficient degradation of poly(A) tails. Involved in nonsense-mediated mRNA decay, a critical process of selective degradation of mRNAs that contain premature stop codons. Also involved in degradation of inherently unstable mRNAs that contain AU-rich elements (AREs) in their 3'-UTR, possibly via its interaction with KHSRP. Probably mediates the removal of poly(A) tails of AREs mRNAs, which constitutes the first step of destabilization (PubMed:10882133, PubMed:11359775, PubMed:12748283, PubMed:15175153, PubMed:9736620).
Also able to recognize and trim poly(A) tails of microRNAs such as MIR21 and H/ACA box snoRNAs (small nucleolar RNAs) leading to microRNAs degradation or snoRNA increased stability (PubMed:25049417, PubMed:22442037).
Biological Process
Box H/ACA RNA 3'-end processingManual Assertion Based On ExperimentIDA:UniProtKB
Female gamete generationManual Assertion Based On ExperimentTAS:ProtInc
miRNA catabolic processManual Assertion Based On ExperimentIDA:UniProtKB
ncRNA deadenylationManual Assertion Based On ExperimentIMP:BHF-UCL
Nuclear-transcribed mRNA catabolic process, nonsense-mediated decayIEA:UniProtKB-KW
Nuclear-transcribed mRNA poly(A) tail shorteningManual Assertion Based On ExperimentIBA:GO_Central
Polyadenylation-dependent snoRNA 3'-end processingManual Assertion Based On ExperimentIDA:UniProtKB
Positive regulation of telomerase activityManual Assertion Based On ExperimentIMP:BHF-UCL
Positive regulation of telomere maintenance via telomeraseManual Assertion Based On ExperimentIMP:BHF-UCL
Regulation of telomerase RNA localization to Cajal bodyManual Assertion Based On ExperimentIMP:BHF-UCL
RNA modificationManual Assertion Based On ExperimentTAS:ProtInc
RNA phosphodiester bond hydrolysis, exonucleolyticManual Assertion Based On ExperimentIMP:BHF-UCL
Telomerase RNA stabilizationManual Assertion Based On ExperimentIMP:BHF-UCL
Cellular Location
Nucleus
Cytoplasm
Nucleus, nucleolus
Some nuclear fraction is nucleolar.
Involvement in disease
Dyskeratosis congenita, autosomal recessive, 6 (DKCB6):
A form of dyskeratosis congenita, a rare multisystem disorder caused by defective telomere maintenance. It is characterized by progressive bone marrow failure, and the clinical triad of reticulated skin hyperpigmentation, nail dystrophy, and mucosal leukoplakia. Common but variable features include premature graying, aplastic anemia, low platelets, osteoporosis, pulmonary fibrosis, and liver fibrosis among others. Early mortality is often associated with bone marrow failure, infections, fatal pulmonary complications, or malignancy.
Pulmonary fibrosis, and/or bone marrow failure, telomere-related, 4 (PFBMFT4):
A disease associated with shortened telomeres. Pulmonary fibrosis is the most common manifestation. Other manifestations include aplastic anemia due to bone marrow failure, hepatic fibrosis, and increased cancer risk, particularly myelodysplastic syndrome and acute myeloid leukemia. Phenotype, age at onset, and severity are determined by telomere length.
PTM
Phosphorylation by MAPKAPK2, preventing GADD45A mRNA degradation after genotoxic stress.
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For research use only. Not intended for any clinical use.

Custom Antibody Labeling

We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).

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