06-937
Anti-phospho-STAT6 (Tyr641) Antibody
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:
western blot
Technique(s):
western blot: suitable
Citations:
9
Uniprot accession no.:
产品名称
Anti-phospho-STAT6 (Tyr641) Antibody, Upstate®, from rabbit
biological source
rabbit
antibody form
purified antibody
antibody product type
primary antibodies
clone
polyclonal
species reactivity
human, mouse
manufacturer/tradename
Upstate®
technique(s)
western blot: suitable
isotype
IgG
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
phosphorylation (pTyr641)
Quality Level
Gene Information
human ... STAT6(6778)
Analysis Note
routinely evaluated by immunoblot on lysates of HepG2 cells, serum starved, then stimulated with IL-4
Application
Research Category
Epigenetics & Nuclear Function
Epigenetics & Nuclear Function
Research Sub Category
Transcription Factors
Transcription Factors
This Anti-phospho-STAT6 (Tyr641) Antibody is validated for use in WB for the detection of phospho-STAT6 (Tyr641).
Biochem/physiol Actions
phospho-STAT6
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.
General description
100kDa
Immunogen
peptide corresponding to amino acids 631-645 of human STAT6 (C-PEQMGKDGRGpYVPAT)
Physical form
0.1M Tris-Glycine, 0.15M NaCl, 0.05% Sodium Azide, pH 7.4.
Format: Purified
Protein A purified
Preparation Note
Maintain at 2-8°C in undiluted aliquots for up to 1 year after date of receipt.
Legal Information
UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany
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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
Defective GATA-3 expression in Th2 LCR-deficient mice.
Soo Seok Hwang,Kiwan Kim,Gap Ryol Lee
Biochemical and biophysical research communications null
F W Quelle et al.
Molecular and cellular biology, 15(6), 3336-3343 (1995-06-01)
By searching a database of expressed sequences, we identified a member of the signal transducers and activators of transcription (Stat) family of proteins. Human and murine full-length cDNA clones were obtained and sequenced. The sequence of the human cDNA was
Giulia Veltri et al.
Cancers, 13(15) (2021-08-08)
Lymphoblastic lymphoma (LBL) is the second most common type of non-Hodgkin lymphoma in childhood, mainly of T cell origin (T-LBL). Although current treatment protocols allow a complete remission in 85% of cases, the second-line treatment overall survival for patients with
Tetsuya Kubota et al.
Nature communications, 9(1), 4863-4863 (2018-11-20)
M2a-subtype macrophage activation is known to be impaired in obesity, although the underlying mechanisms remain poorly understood. Herein, we demonstrate that, the IL-4/Irs2/Akt pathway is selectively impaired, along with decreased macrophage Irs2 expression, although IL-4/STAT6 pathway is maintained. Indeed, myeloid
Jason C O'Connor et al.
Journal of immunology (Baltimore, Md. : 1950), 178(11), 6886-6893 (2007-05-22)
Chronic elevation of proinflammatory markers in type 2 diabetes (T2D) is well defined, but the role of anti-inflammatory cytokines in T2D is less clear. In this study, we report that normal IL-4-dependent elaboration of IL-1 receptor antagonist (IL-1RA) requires IRS-2-mediated
相关内容
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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