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Key Documents

06-891

Sigma-Aldrich

Anti-SMRTe Antibody

Upstate®, from rabbit

Synonym(s):

Anti-CTG26, Anti-N-CoR2, Anti-SMAP270, Anti-SMRT, Anti-SMRTE, Anti-SMRTE-tau, Anti-TNRC14, Anti-TRAC, Anti-TRAC-1, Anti-TRAC1

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About This Item

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

biological source

rabbit

Quality Level

antibody form

purified antibody

antibody product type

primary antibodies

clone

polyclonal

species reactivity

human

manufacturer/tradename

Upstate®

technique(s)

ChIP: suitable
immunocytochemistry: suitable
western blot: suitable

isotype

IgG

NCBI accession no.

UniProt accession no.

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

General description

SMRT is 1495 amino acids and contains an 8 amino acid sequence that is not present in SMRTe (SMRT-extended), which contains 2514 amino acids. SMRTe contains an N-terminal sequence spanning over 1,000 amino acids that is not present in SMRT, but that shows significant similarity with N-CoR. SMRTe expression is regulated during cell cycle progression, suggesting a role for SMRTe in the regulation of cycle-specific gene expression in diverse signaling pathways.

Specificity

SMRT isoforms

Immunogen

GST fusion-protein corresponding to residues 1146-1349 of human SMRTe

Application

Anti-SMRTe Antibody is a high quality Rabbit Polyclonal Antibody for the detection of SMRTe & has been validated in ChIP, ICC & WB.
Research Category
Protein Trafficking

Epigenetics & Nuclear Function
Research Sub Category
RNA Metabolism & Binding Proteins

Histones

RNA Binding Protein (RBP)

Quality

routinely evaluated by immunoblot on nuclear fraction from murine brain

Target description

270kDa, 180kDa and 80kDa

Physical form

0.1M Tris-glycine, pH 7.4, 0.15M NaCl, 0.05% sodium azide before the addition of glycerol to 30%
Format: Purified
Protein A chromatography

Storage and Stability

Store at 2–8°C

Analysis Note

Control
Mouse brain nuclear extract

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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Storage Class Code

12 - Non Combustible Liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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TGF-? and retinoic acid induce the microRNA miR-10a, which targets Bcl-6 and constrains the plasticity of helper T cells.
Takahashi, H; Kanno, T; Nakayamada, S; Hirahara, K; Sciume, G; Muljo, SA; Kuchen et al.
Nature Immunology null
The Flt3 internal tandem duplication mutant inhibits the function of transcriptional repressors by blocking interactions with SMRT.
Takahashi, S; McConnell, MJ; Harigae, H; Kaku, M; Sasaki, T; Melnick, AM; Licht, JD
Blood null
Hiroaki Shimizu et al.
PloS one, 14(8), e0220717-e0220717 (2019-08-14)
Silencing Mediator of Retinoid and Thyroid Hormone Receptors (SMRT) and the nuclear receptor co-repressor1 (NCoR1) are paralogs and regulate nuclear receptor (NR) function through the recruitment of a multiprotein complex that includes histone deacetylase activity. Previous genetic strategies which deleted
Megan J Ritter et al.
Molecular metabolism, 53, 101315-101315 (2021-08-15)
The nuclear receptor corepressor 1 (NCOR1) and the silencing mediator of retinoic acid and thyroid hormone (SMRT, also known as NCOR2) play critical and specific roles in nuclear receptor action. NCOR1, both in vitro and in vivo specifically regulates thyroid hormone (TH)
Dong Wook Kim et al.
Human molecular genetics, 23(10), 2651-2664 (2014-01-02)
Mutations of the thyroid hormone receptor α gene (THRA) cause hypothyroidism in patients with growth and developmental retardation, and skeletal dysplasia. Genetic evidence indicates that the dominant negative activity of TRα1 mutants underlies pathological manifestations. Using a mouse model of

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