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MEF2C Antibody Features in Nature Biotechnology

admin February 26, 2013
Immunohistochemistry of paraffin-embedded lymphoma tissue using Proteintech's anti-MEF2C antibody 10056-1-AP (viewed under 40x lens).

Immunohistochemistry of paraffin-embedded lymphoma tissue using Proteintech’s anti-MEF2C antibody 10056-1-AP (viewed under 40x lens).

Myocyte-specific enhancer factor 2, encoded by the MEF2C gene, is a well-established transcription factor involved in skeletal, cardiac and smooth muscle cell development. More recently, its role in brain development and function has also entered the research spotlight; the importance of MEF2C has been demonstrated in neural stem cells (NSCs), and by the observation of autism spectrum disorder (ASD)-like phenotypes following NSC-specific knockout of Mef2c in mice. The role of MEF2C in brain development is further supported by the existence of patients with severe learning difficulties, epilepsy and cerebral malformations whom also harbor deletions in the chromosomal region where MEF2C is located. Further genetic work with these patients has shown that MEF2C is the likely gene affected [1].

It’s no surprise that MEF2C protein expression is vital for the development and correct function of an array of important tissues as it plays a role in neural crest cell development during embryogenesis [2 and 3]. Neural crest cells are multipotent cells that undergo an epithelial-to-mesenchymal transition as they migrate from their site of origin to different locations in the developing embryo. This process gives rise to a variety of different cell types, including: neurons, chondrocytes, osteocytes, melanocytes, hormone-producing cells, as well as the cell types introduced earlier. Absence of this protein has serious consequences, which have been demonstrated in mice; loss of Mef2c in mouse neural crest cells results in neonatal lethality due to severe craniofacial defects that obstruct the upper airways [4].

SH-SY5Y cell lysates were separated by SDS-PAGE and MEF2C protein was detected by Western blotting with Proteintech's anti-MEF2C Antibody 10056-1-AP.

SH-SY5Y cell lysates were separated by SDS-PAGE and MEF2C protein was detected by Western blotting with Proteintech’s anti-MEF2C Antibody 10056-1-AP.

Proteintech’s anti-MEF2C antibody has recently featured in a Nature Biotechnology article examining and utilizing the differences between cell-types of the early developing embryo. The paper describes the isolation of primitive endoderm, mesoderm, vascular endothelial and trophoblast progenitors from human pluripotent stem cells. In this body of work, the Proteintech MEF2C antibody was included in a panel of marker antibodies used to distinguish mesoderm tissue by immunostaining. It was also used for the immunohistochemical staining of mouse kidney capsule injected with cell grafts of human ROR2+ cells. Presence of MEF2C along with several other mesoderm markers (GATA4, SMA and CD31) in ROR2+ cell populations indicated differentiation towards mesenchymal mesoderm tissue.

The ROR2 gene encodes a tyrosine-protein kinase transmembrane receptor, involved in primitive streak formation in the developing embryo. Cell populations positive for this receptor change their gene expression in the presence of bone morphogenetic protein 4 (BMP4) and there is evidence to suggest BMP4 induces emergence of trophoblasts from human embryonic stem cells (hESCs). However, this was recently challenged by a report suggesting that BMP4-treated hESCs are actually mesoderm cells expressing trophoblast genes [5]. The recent work presented in Nature Biotechnology is consistent with this theory, and is supported by the involvement of ROR2 in early mesoderm development.

More on Proteintech’s anti-MEF2C antibody

In addition to immunostaining mesodermal tissue, Proteintech’s anti-MEF2C antibody has also featured in several journal papers utilizing it to detect a variety of other tissue and cell types including lateral amygdala, Mef2c+ neurons and differentiated cardiac muscle.

Find further  details in these PubMed referenced articles: 22634564, 22492355, 22337869, 21666133, 21471366, 20484636, 20221419, 19696409

References

[1] F. Novara et al., Clinical Genetics 2010; 78(5):471-477

[2] M.J. Potthoff and E.N. Olson, Development 2007;134:4131-4140

[3] A.K. Knecht and M. Bronner-Fraser Nat. Rev. Genet. 2005;3:453-461

[4] M.P. Verzi et al., Dev. Cell 2007;12:645-652

[5] M Drukker et al., Nature Biotechnology 2012;30(6):531-42

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