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Anti-LSD1/BHC110, Cat. No. 05-939-I, is a mouse monoclonal antibody that detects Lysine-specific histone demethylase 1A and is tested for use in Chromatin Immunoprecipitation (ChIP), Immunocytochemistry, and Western Blotting.
More>>Anti-LSD1/BHC110, Cat. No. 05-939-I, is a mouse monoclonal antibody that detects Lysine-specific histone demethylase 1A and is tested for use in Chromatin Immunoprecipitation (ChIP), Immunocytochemistry, and Western Blotting. Less<<
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Übersicht
Replacement Information
Description
Catalogue Number
05-939-I-100UL
Description
Anti-LSD1/BHC110 Antibody, clone Clone AP06.20
Alternate Names
Lysine-specific histone demethylase 1A
BRAF35-HDAC complex protein BHC110
Flavin-containing amine oxidase domain-containing protein 2
Background Information
Lysine-specific histone demethylase 1A (UniProt: O60341; also known as BRAF35-HDAC complex protein BHC110, Flavin-containing amine oxidase domain-containing protein 2, LSD1) is encoded by the KD1MA (also known as AOF2, KDM1, KIAA0601, LSD1) gene (Gene ID: 23028) in human. LSD1 is a ubiquitously expressed histone demethylase that can demethylate both lysine 4 (H3K4me) and lysine 9 (H3K9me) of histone H3, thereby acting as a coactivator or a corepressor. It is a component of a RCOR/GFI/KDM1A/HDAC complex that suppresses several genes implicated in multilineage blood cell development. It acts by oxidizing the substrate by FAD to generate the corresponding imine that is subsequently hydrolyzed. It can also act as a corepressor by mediating demethylation of mono- and di-methylated H3K4me, a specific tag for epigenetic transcriptional activation. It has been reported that alone it is not able to demethylate H3K4me on nucleosomes and requires the presence of RCOR1/CoREST to achieve such activity. LSD1 is also shown to act as a coactivator of androgen receptor (ANDR)-dependent transcription, by being recruited to ANDR target genes and mediating demethylation of H3K9me, a specific tag for epigenetic transcriptional repression. LSD1 is also involved in demethylation of lysine 370 on p53/TP53 that blocks interaction of p53/TP53 with TP53BP1 and represses p53/TP53-mediated transcriptional activation. Two isoforms of LSD1 have been described that are produced by alternative splicing.
References
Product Information
Format
Purified
Presentation
Purified mouse monoclonal antibody IgG in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.
Anti-LSD1/BHC110, Cat. No. 05-939-I, is a mouse monoclonal antibody that detects Lysine-specific histone demethylase 1A and is tested for use in Chromatin Immunoprecipitation (ChIP), Immunocytochemistry, and Western Blotting.
Key Applications
Chromatin Immunoprecipitation (ChIP)
Immunocytochemistry
Western Blotting
Application Notes
Western Blotting Analysis: A 1:1,000 dilution from a representative lot detected LSD1/BHC110 in HEK293 cell nuclear extract.
Chromatin Immunoprecipitation (ChIP) Analysis: A representative lot detected LSD1/BHC110 in Chromatin Immunoprecipitation applications (Brasacchio, D., et. al. (2009). Diabetes. 58(5):1229-36).
Immunocytochemistry Analysis: A 1:250 dilution from a representative lot detected LSD1/BHC110 in HeLa cells.
Note: Actual optimal working dilutions must be determined by end user as specimens, and experimental conditions may vary with the end user
Biological Information
Immunogen
GST-tagged recombinant fragment corresponding to 116 amino acids from the N-terminal half of human Lysine-specific histone demethylase 1A (LSD1/BHC110).
Epitope
N-terminus
Clone
AP06.20
Concentration
0.5 mg/mL. Please refer to guidance on suggested starting dilutions and/or titers per application and sample type.
Host
Mouse
Specificity
Clone AP06.20 is a mouse monoclonal antibody that detects Lysine-specific histone demethylase 1A (LSD1). It targets an epitope within the N-terminal half.
Isotype
IgG
Species Reactivity
Human
Species Reactivity Note
Human. Predicted to react with Mouse based on 100% sequence homology.
~110 kDa observed; 92.90 kDa calculated. Uncharacterized bands may be observed in some lysate(s).
Physicochemical Information
Dimensions
Materials Information
Toxicological Information
Safety Information according to GHS
Safety Information
Product Usage Statements
Quality Assurance
Evaluated by Western Blotting in Hela cell nuclear extract.
Western Blotting Analysis: A 1:1,000 dilution of this antibody detected LSD1/BHC110 in HeLa cell nuclear extract.
Usage Statement
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.
Storage and Shipping Information
Storage Conditions
Stable for 1 year at +2°C to +8°C from date of receipt.
Hyperglycemia induces a dynamic cooperativity of histone methylase and demethylase enzymes associated with gene-activating epigenetic marks that coexist on the lysine tail Daniella Brasacchio 1 , Jun Okabe, Christos Tikellis, Aneta Balcerczyk, Prince George, Emma K Baker, Anna C Calkin, Michael Brownlee, Mark E Cooper, Assam El-Osta Diabetes
58(5)
1229-36
2009
Objective: Results from the Diabetes Control Complications Trial (DCCT) and the subsequent Epidemiology of Diabetes Interventions and Complications (EDIC) Study and more recently from the U.K. Prospective Diabetes Study (UKPDS) have revealed that the deleterious end-organ effects that occurred in both conventional and more aggressively treated subjects continued to operate >5 years after the patients had returned to usual glycemic control and is interpreted as a legacy of past glycemia known as "hyperglycemic memory." We have hypothesized that transient hyperglycemia mediates persistent gene-activating events attributed to changes in epigenetic information. <br />Research design and methods: Models of transient hyperglycemia were used to link NFkappaB-p65 gene expression with H3K4 and H3K9 modifications mediated by the histone methyltransferases (Set7 and SuV39h1) and the lysine-specific demethylase (LSD1) by the immunopurification of soluble NFkappaB-p65 chromatin. <br />Results: The sustained upregulation of the NFkappaB-p65 gene as a result of ambient or prior hyperglycemia was associated with increased H3K4m1 but not H3K4m2 or H3K4m3. Furthermore, glucose was shown to have other epigenetic effects, including the suppression of H3K9m2 and H3K9m3 methylation on the p65 promoter. Finally, there was increased recruitment of the recently identified histone demethylase LSD1 to the p65 promoter as a result of prior hyperglycemia. <br />Conclusions: These studies indicate that the active transcriptional state of the NFkappaB-p65 gene is linked with persisting epigenetic marks such as enhanced H3K4 and reduced H3K9 methylation, which appear to occur as a result of effects of the methyl-writing and methyl-erasing histone enzymes.
