Antibody studies into human CHARGE syndrome have shown mutated CHD7 plays a major role in its development. CHARGE originates in neural crest cells (NCCs) during early embryonic development. It leads to a number of birth defects including craniofacial, heart, brain, urogenital, hearing and growth defects. New research conducted by Wysocka et al, of the Stamford University School of Medicine, indicates a connection with tumour development in adults.
Chromatin is the tightly-packed form of DNA found within the cell nucleus. It is controlled by a number of chromatin remodeler proteins, one of which is CHD7. CHD7 acts on nuclear proteins to allow activation or deactivation of various genes.
NCCs are unusual in that they migrate freely during embryonic development, differentiating into a range of cells including neural, heart, cartilage and bone cells. Wysocka et al, of the Stamford University School of Medicine, recently conducted antibody assays exploring the critical role CHD7 plays within neural crest cells.
Immunohistochemistry: Chd7 Antibody
Previous studies had showed mutated CHD7 was expressed in CHARGE cells. By blocking CHD7 release in tadpoles, cell migration was halted and symptoms similar to those of CHARGE sufferers were expressed, proving that uncorrupted CHD7 is essential to normal embryonic development.
Further antibody studies showed CHD7 worked in combination with the PBAF chromatin remodelling complex, to control remote genes. Previous studies have shown that Slug and Twist - two genes controlled by CHD7 and PBAF - are oncogenic.
Novus Biologicals offers many CHD7 reagents for your research needs including:
