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Key Documents

MABE302

Sigma-Aldrich

Anti-2,2,7-Trimethylguanosine Antibody, clone K121

clone K121, from mouse

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About This Item

Code UNSPSC :
12352203
eCl@ss :
32160702
Nomenclature NACRES :
NA.41

Source biologique

mouse

Niveau de qualité

Forme d'anticorps

purified immunoglobulin

Type de produit anticorps

primary antibodies

Clone

K121, monoclonal

Espèces réactives

human, mouse

Technique(s)

affinity chromatography: suitable
immunocytochemistry: suitable
immunoprecipitation (IP): suitable

Isotype

IgG1κ

Conditions d'expédition

wet ice

Modification post-traductionnelle de la cible

unmodified

Description générale

The 2,2,7-trimethylguanosine cap structure is found on the 5’ end of small nuclear RNAs and small nucleolar RNAs. Initially, these RNA molecules are capped with 7-monomethylguanosine (m7G) which is then methylated by the trimethylguanosine synthase enzyme to form 2,2,7-trimethylguanosine. The synthesis of 2,2,7-trimethylguanosine occurs in the cytoplasm and is an important marker for nuclear localization of RNA molecules. Capping of RNAs is an important requirement for RNA transport and splicing processes. Uncapped RNAs are rapidly degraded by the 5′ exoribonuclease enzyme. 2,2,7-trimethylguanosine capping may play a role in the expression of viral RNAs.

Application

Anti-2, 2, 7-Trimethylguanosine Antibody, clone K121 is a high quality Mouse Monoclonal Antibody for the detection of 2, 2, 7-Trimethylguanosine & has been validated in ICC, PAI & IP.
Immunoaffinity Purification Analysis: A representative lot from an independent laboratory was used in IAP (Krainer, A.R., et al. (1988). Nucleic Acids Res. 16(20):9415-9429.).

Immunoprecipitation Analysis: A representative lot from an independent laboratory was immunoprecipitated in IP (Moketi, S., et al. (2002). Mol Cell. 10(3):599-609.).

Qualité

Evaluated by Immunocytochemistry in NIH/3T3, HeLa, and A431 cells.

Immunocytochemistry Analysis: A 1:500 dilution of this antibody detected 2,2,7-trimethylguanosine in NIH/3T3, HeLa, and A431 cells.

Forme physique

Format: Purified

Remarque sur l'analyse

Control
NIH/3T3, HeLa, and A431 cells

Autres remarques

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

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Code de la classe de stockage

12 - Non Combustible Liquids

Classe de danger pour l'eau (WGK)

WGK 1

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.

Consulter la Bibliothèque de documents

Cyrille Girard et al.
Nucleic acids research, 34(10), 2925-2932 (2006-06-02)
Neuronal degeneration in spinal muscular atrophy (SMA) is caused by reduced expression of the survival of motor neuron (SMN) protein. The SMN protein is ubiquitously expressed and is present both in the cytoplasm and in the nucleus where it localizes
Magdalena Strzelecka et al.
Nucleus (Austin, Tex.), 1(1), 96-108 (2011-02-18)
The Cajal body (CB) is an evolutionarily conserved nuclear subcompartment, enriched in components of the RNA processing machinery. The composition and dynamics of CBs in cells of living organisms is not well understood. Here we establish the zebrafish embryo as
Pre-mRNA splicing by complementation with purified human U1, U2, U4/U6 and U5 snRNPs.
Krainer, A R
Nucleic Acids Research, 16, 9415-9429 (1988)
Cristina Moreno-Castro et al.
Journal of cell science, 132(22) (2019-10-23)
Cajal bodies are nuclear organelles involved in the nuclear phase of small nuclear ribonucleoprotein (snRNP) biogenesis. In this study, we identified the splicing factor TCERG1 as a coilin-associated factor that is essential for Cajal body integrity. Knockdown of TCERG1 disrupts
Masaki Kobayashi et al.
Disease models & mechanisms, 10(3), 215-224 (2017-03-03)
Unique deficits in the function of adult sensory neurons as part of their early neurodegeneration might account for progressive polyneuropathy during chronic diabetes mellitus. Here, we provide structural and functional evidence for aberrant pre-mRNA splicing in a chronic type 1

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