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07-551

Sigma-Aldrich

Anti-G9a Antibody

Upstate®, from rabbit

Synonym(s):

KMT1C

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About This Item

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

biological source

rabbit

Quality Level

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

polyclonal

species reactivity

human

packaging

antibody small pack of 25 μg

manufacturer/tradename

Upstate®

technique(s)

western blot: suitable

isotype

IgG

NCBI accession no.

UniProt accession no.

shipped in

dry ice

target post-translational modification

unmodified

Gene Information

human ... EHMT2(10919)

General description

Protein G9a (also known as Histone H3-K9 methyltransferase 3, Euchromatic histone-lysine N-methyltransferase 2 and HLA-B-associated transcript 8)

Specificity

Recognizes human G9a protein.

Immunogen

Peptide (C-DERVDSDSKSEVEALTEQ) corresponding to amino acids 71-88 of human G9a.

Application

Research Category
Epigenetics & Nuclear Function
Research Sub Category
Histones
Use Anti-G9a Antibody (Rabbit Polyclonal Antibody) validated in WB to detect G9a also known as KMT1C.

Quality

routinely evaluated by immunoblot HeLa nuclear extract cell lysate

Target description

140 kDa

Physical form

Format: Purified
Protein A Purified immunoglobulin in 30% glycerol, 0.07M Tris-glycine, pH 7.4, 0.105 M NaCl, 0.035% sodium azide as a preservative.
Protein A purified

Storage and Stability

Maintain for 2 years at -20°C from date of shipment. Aliquot to avoid repeated freezing and thawing. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.

Analysis Note

Control
Positive Antigen Control: Catalog #12-309, Hela cell nuclear extract. Add an equal volume of Laemmli reducing sample buffer to 10 μL of extract and boil for 5 minutes to reduce the preparation. Load 20 μg of reduced extract per lane for minigels.
Control
Positive Control Included: HeLa Nuclear Extract (12-309).

Other Notes

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

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

10 - Combustible liquids

WGK

WGK 2


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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Role of the PLDLS-binding cleft region of CtBP1 in recruitment of core and auxiliary components of the corepressor complex.
Kuppuswamy, M; Vijayalingam, S; Zhao, LJ; Zhou, Y; Subramanian, T; Ryerse, J; Chinnadurai, G
Molecular and cellular biology null
Changes in C-terminal binding protein 2 (CtBP2) corepressor complex induced by E1A and modulation of E1A transcriptional activity by CtBP2.
Zhao, LJ; Subramanian, T; Chinnadurai, G
The Journal of Biological Chemistry null
Gfi1 coordinates epigenetic repression of p21Cip/WAF1 by recruitment of histone lysine methyltransferase G9a and histone deacetylase 1.
Duan, Z; Zarebski, A; Montoya-Durango, D; Grimes, HL; Horwitz, M
Molecular and cellular biology null
Mihai G Mehedint et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 24(1), 184-195 (2009-09-16)
Maternal choline availability is essential for fetal neurogenesis. Choline deprivation (CD) causes hypomethylation of specific CpG islands in genes controlling cell cycling in fetal hippocampus. We now report that, in C57BL/6 mice, CD during gestational days 12-17 also altered methylation
Gene repressive activity of RIP140 through direct interaction with CDK8.
Persaud, SD; Huang, WH; Park, SW; Wei, LN
Molecular Endocrinology null

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