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Merck
CN

06-1040

Anti-RIG-I (NT) Antibody

from rabbit, purified by affinity chromatography

别名:

Probable ATP-dependent RNA helicase DDX58, DEAD box protein 58, Retinoic acid-inducible gene 1 protein, RIG-1, Retinoic acid-inducible gene I protein, RIG-I

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关于此项目

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

rabbit

Quality Level

antibody product type

primary antibodies

clone

polyclonal

purified by

affinity chromatography

species reactivity

human

technique(s)

immunoprecipitation (IP): suitable, western blot: suitable

NCBI accession no.

UniProt accession no.

shipped in

wet ice

General description

Retinoic acid-inducible gene 1 protein (RIG-1) is a cytoplasmic DExD/H box RNA helicase belonging to the helicase family and containing 2 CARD domains within the N-terminus, a repressor domain (RD), a helicase ATP-binding domain and a helicase C-terminal binding domain. RIG-1 is able to bind the 5’-triphosphate RNA of single or double-stranded viral RNA. After recognizing and binding viral RNA, RIG-1 protein initializes type I IFN production, and within fibroblasts and dendritic cells plays a central role in the regulation of type I IFN production in response to viral presence. There are four known isoforms resulting from alternative splice variants.
~102 kDa observed

Immunogen

Epitope: N-terminus
GST-tagged recombinant protein corresponding to the N-terminus of human RIG-I.

Application

Immunoprecipitation Analysis: A representative lot was used by an independent laboratory in IP. (Paz, S., et al. (2011). Cell Research. 1-16.)
Research Category
Inflammation & Immunology
Research Sub Category
Immunoglobulins & Immunology
Use Anti-RIG-I (N-Terminus) Antibody (Rabbit Polyclonal Antibody) validated in WB, IP to detect RIG-I (N-Terminus) also known as Retinoic acid-inducible gene 1 protein.

Biochem/physiol Actions

Other homologies: Rhesus Monkey (99% sequence homology).
This antibody recognizes RIG-I at the N-terminus.

Physical form

Affinity purified
Purified rabbit polyclonal in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Preparation Note

Stable for 1 year at 2-8°C from date of receipt.

Analysis Note

Control
SeV treated and untreated A549 cell lysates
Evaluated by Western Blot in SeV treated and untreated A549 cell lysates.

Western Blot Analysis: 0.05 µg/mL of this antibody detected RIG-I on 10 µg of SeV untreated and treated A549 cell lysates.

Other Notes

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

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.


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存储类别

12 - Non Combustible Liquids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable



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A functional C-terminal TRAF3-binding site in MAVS participates in positive and negative regulation of the IFN antiviral response.
Paz, S; Vilasco, M; Werden, SJ; Arguello, M; Joseph-Pillai, D; Zhao, T; Nguyen, TL; Sun et al.
Cell research null
Silvia Albertini et al.
Journal of immunology (Baltimore, Md. : 1950), 200(6), 2076-2089 (2018-02-02)
Although it is clear that high-risk human papillomaviruses (HPVs) can selectively infect keratinocytes and persist in the host, it still remains to be unequivocally determined whether they can escape antiviral innate immunity by interfering with pattern recognition receptor (PRR) signaling.
Irene Lo Cigno et al.
Journal of virology, 94(4) (2019-11-30)
Subversion of innate immunity by oncoviruses, such as human papillomavirus (HPV), favors carcinogenesis because the mechanism(s) of viral immune evasion can also hamper cancer immunosurveillance. Previously, we demonstrated that high-risk (hr) HPVs trigger simultaneous epigenetic silencing of multiple effectors of