Disease relevance of NLRP7

• Mutations in NALP7 cause recurrent hydatidiform moles and reproductive wastage in humans [1].
• NALP7 is the first maternal effect gene identified in humans and is also responsible for recurrent spontaneous abortions, stillbirths and intrauterine growth retardation [1].
• Oncogenic role of NALP7 in testicular seminomas [2].
• Immunohistochemical analysis using anti-NALP7 polyclonal antibody detected the endogenous NALP7 protein in the cytoplasm of embryonal carcinoma cells and testicular seminoma tissues [2].

High impact information on NLRP7

• NALP7 is a member of the CATERPILLER protein family involved in inflammation and apoptosis [1].
• Stimulation of monocytic THP-1 cells with lipopolysaccharide or interleukin-1beta induced PYPAF3 mRNA expression [3].
• Both PYPAF2 and PYPAF3 mRNAs are broadly expressed in a variety of tissues; however, neither is expressed in skeletal muscle, and only PYPAF2 mRNA is expressed in heart and brain [3].
• Familial molar tissues due to mutations in the inflammatory gene, NALP7, have normal postzygotic DNA methylation [4].
• The known role of NALP7 in apoptosis and inflammation pinpoints previously unrecognized pathways that could directly or indirectly underlie the abnormal methylation of imprinted genes in molar tissues [4].

Chemical compound and disease context of NLRP7

• We here report identification of NACHT, leucine-rich repeat and PYD containing 7 (NALP7 ), that was significantly transactivated in testicular seminomas [2].

Biological context of NLRP7

• These findings imply that NALP7 may play a crucial role in cell proliferation, as well as testicular tumorigenesis, and it appears to be a promising candidate for development of targeted therapy for TGCTs [2].
• Transfection of small interfering RNA (siRNA) for NALP7 significantly reduced the NALP7 expression and resulted in growth suppression of testicular germ-cell tumors [2].
• NALP7 could have a role either in oogenesis or in the endometrium during trophoblast invasion and decidualization [5].

Other interactions of NLRP7

• Additionally, pro-apoptosis genes were down-regulated (e.g. twofold for CASP1, 2.5-fold for NALP7) with concomitant increased expression of the potential anti-apoptosis gene AKT3 [6].

References