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Merck
CN

06-502

Anti-STAT2 Antibody, CT

Upstate®, from rabbit

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关于此项目

UNSPSC Code:
12352203
NACRES:
NA.41
eCl@ss:
32160702
Clone:
polyclonal
Species reactivity:
human, mouse
Application:
EMSA, ICC, IP, WB
Citations:
17
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biological source

rabbit

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

polyclonal

species reactivity

human, mouse

manufacturer/tradename

Upstate®

technique(s)

electrophoretic mobility shift assay: suitable, immunocytochemistry: suitable, immunoprecipitation (IP): suitable, western blot: suitable

isotype

IgG

NCBI accession no.

UniProt accession no.

shipped in

wet ice

Quality Level

Gene Information

human ... STAT2(6773)

General description

113kDa

Immunogen

GST fusion protein containing amino acids 671-806 of human STAT2

Application

Anti-STAT2 Antibody, CT is a Rabbit Polyclonal Antibody for detection of STAT2 also known as Signal Transducer & Activator of Transcription 2 & has been tested in EMSA, IP, WB, ICC.
Research Category
Epigenetics & Nuclear Function
Research Sub Category
Transcription Factors

Biochem/physiol Actions

STAT2

Physical form

0.07 M Tris-glycine, pH 7.4, 0.105 M NaCl, 0.035% sodium azide and 30% glycerol.
Format: Purified
Protein A chromatography

Preparation Note

2 years at -20°C

Analysis Note

Immunoblot Analysis: 0.5-2 μg/ml of this antibody detected STAT2 (113kDa) in Jurkat cell lysates.

Legal Information

UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany

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

10 - Combustible liquids

wgk

WGK 1


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Alicia L Humlicek et al.
Journal of immunology (Baltimore, Md. : 1950), 178(10), 6395-6403 (2007-05-04)
Respiratory pathogens and toxins often assault the lung from the airway lumen. Airway epithelia may initiate and amplify inflammation in response to these attacks, but under certain conditions confinement of inflammation to the airway lumen may be beneficial to the
Marta Martin-Fernandez et al.
Cell reports, 31(6), 107633-107633 (2020-05-14)
Most monogenic disorders have a primary clinical presentation. Inherited ISG15 deficiency, however, has manifested with two distinct presentations to date: susceptibility to mycobacterial disease and intracranial calcifications from hypomorphic interferon-II (IFN-II) production and excessive IFN-I response, respectively. Accordingly, these patients
Conor Gruber et al.
The Journal of experimental medicine, 217(5) (2020-02-25)
Type I interferonopathies are monogenic disorders characterized by enhanced type I interferon (IFN-I) cytokine activity. Inherited USP18 and ISG15 deficiencies underlie type I interferonopathies by preventing the regulation of late responses to IFN-I. Specifically, USP18, being stabilized by ISG15, sterically
The nucleocytoplasmic rabies virus P protein counteracts interferon signaling by inhibiting both nuclear accumulation and DNA binding of STAT1.
Vidy, A; El Bougrini, J; Chelbi-Alix, MK; Blondel, D
Journal of virology null
Gang Ren et al.
Cell & bioscience, 5, 17-17 (2015-05-12)
Cellular antiviral activities are critically controlled by transcriptional activation of interferon-inducible genes, involving interferon regulatory factors (IRFs). Previous data suggested that IRF1 is an activator and IRF2 is a repressor, which functionally antagonize each other in transcriptional regulation. However, it

相关内容

Pathways and Biomarkers of JAK/STAT Signaling

The Janus kinase (JAK)/signal transducers and activators of transcription (STAT) signaling pathway plays an important role in cell proliferation, cell differentiation, cell migration, and cell death. It is the principal signaling mechanism for a variety of cytokines and growth factors. Constitutive activation or dysregulation of JAK/STAT signaling can result in inflammatory disease, erythrocytosis, gigantism, and leukemia.

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