SAB1401241
Anti-MEF2C antibody produced in mouse
purified immunoglobulin, buffered aqueous solution
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About This Item
UNSPSC Code:
12352203
NACRES:
NA.41
biological source
mouse
Quality Level
conjugate
unconjugated
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
species reactivity
human
technique(s)
western blot: 1 μg/mL
NCBI accession no.
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... MEF2C(4208)
Immunogen
MEF2C (AAH26341.1, 1 a.a. ~ 469 a.a) full-length human protein.
Sequence
MGRKKIQITRIMDERNRQVTFTKRKFGLMKKAYELSVLCDCEIALIIFNSTNKLFQYASTDMDKVLLKYTEYNEQHESRTNSDIVETLRKKGLNGCDSPDPDADDSVGHSPESEDKYRKINEDIDLMISRQRLCAVPPPNFEMPVSIPVSSHNSLVYSNPVSSLGNPNLLPLAHPSLQRNSMSPGVTHRPPSAGNTGGLMGGDLTSGAGTSAGNGYGNPRNSPGLLVSPGNLNKNMQAKSPPPMNLGMNNRKPDLRVLIPPGSKNTMPSVSEDVDLLLNQRINNSQSAQSLATPVVSVATPTLPGQGMGGYPSAISTTYGTEYSLSSADLSSLSGFNTASALHLGSVTGWQQQHLHNMQPSALSQLGACTSTHLSQSSNLSLPSTQSLNIKSEPVSPPRDRTTTPSRYPQHTRHEAGRSPVDSLSSCSSSYDGSDREDHRNEFHSPIGLTRPSPDERESPSVKRMRLSE
Sequence
MGRKKIQITRIMDERNRQVTFTKRKFGLMKKAYELSVLCDCEIALIIFNSTNKLFQYASTDMDKVLLKYTEYNEQHESRTNSDIVETLRKKGLNGCDSPDPDADDSVGHSPESEDKYRKINEDIDLMISRQRLCAVPPPNFEMPVSIPVSSHNSLVYSNPVSSLGNPNLLPLAHPSLQRNSMSPGVTHRPPSAGNTGGLMGGDLTSGAGTSAGNGYGNPRNSPGLLVSPGNLNKNMQAKSPPPMNLGMNNRKPDLRVLIPPGSKNTMPSVSEDVDLLLNQRINNSQSAQSLATPVVSVATPTLPGQGMGGYPSAISTTYGTEYSLSSADLSSLSGFNTASALHLGSVTGWQQQHLHNMQPSALSQLGACTSTHLSQSSNLSLPSTQSLNIKSEPVSPPRDRTTTPSRYPQHTRHEAGRSPVDSLSSCSSSYDGSDREDHRNEFHSPIGLTRPSPDERESPSVKRMRLSE
Biochem/physiol Actions
MEF2C (myocyte enhancer factor 2C) is a cardiac and smooth muscle-specific transcription factor. It positively regulates the transcriptional activation induced by myocardin. Thus, it coordinates the smooth muscle cell differentiation. MEF2C is associated with nuclear factor of activated T-cells (NFAT) and upregulation of the gene is observed in mitral regurgitation. In retina, the MEF2C regulates the expression of photoreceptor gene.
Physical form
Solution in phosphate buffered saline, pH 7.4
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
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
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Markus Zweier et al.
Human mutation, 31(6), 722-733 (2010-06-01)
The etiology of mental retardation remains elusive in the majority of cases. Microdeletions within chromosomal bands 5q14.3q15 were recently identified as a recurrent cause of severe mental retardation, epilepsy, muscular hypotonia, and variable minor anomalies. By molecular karyotyping we identified
Sanghamitra Sahoo et al.
PloS one, 11(5), e0153780-e0153780 (2016-05-06)
Vascular hyperproliferative disorders are characterized by excessive smooth muscle cell (SMC) proliferation leading to vessel remodeling and occlusion. In pulmonary arterial hypertension (PAH), SMC phenotype switching from a terminally differentiated contractile to synthetic state is gaining traction as our understanding
Retinal expression and localization of Mef2c support its important role in photoreceptor gene expression.
Wolf A
Biochemical and Biophysical Research Communications, 483(1), 346-351 (2017)
Tzu-Hao Chang et al.
PloS one, 11(12), e0166791-e0166791 (2016-12-03)
Left atrial enlargement in mitral regurgitation (MR) predicts a poor prognosis. The regulatory mechanisms of atrial myocyte hypertrophy of MR patients remain unknown. This study comprised 14 patients with MR, 7 patients with aortic valve disease (AVD), and 6 purchased
Mutations in MEF2C from the 5q14.3q15 microdeletion syndrome region are a frequent cause of severe mental retardation and diminish MECP2 and CDKL5 expression.
Zweier M
Human Mutation, 31(6), 722-733 (2010)
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