It is also interesting to note that the Sema3a gene knockout mouse shows very wide foot processes and foot process effacement. Our array data showed that Sema3a is expressed during kidney development, but is turned off in the adult podocyte. In contrast, Sema3e and Sema3g were off during development and expressed in the adult. Sema5a was expressed at low levels during development and strongly in the adult. Podocytes also expressed the Mertk gene, encoding a receptor kinase, which is of interest in terms of the possible clearing role of podocytes, since this gene has been shown to be important in the phagocytic AbMole Oxytocin Syntocinon function of some cell types. Podocytes also expressed Colec12a scavenger receptor that has been shown to be important in the mediation of zymosan phagocytosis by vascular endothelial cells. It has also been implicated in the clearance of amyloid beta in Alzheimers disease. Other signaling molecules of particular interest expressed by podocytes included Spred2, which is a sprouty related inhibitor of receptor tyrosine kinases, and Gmfb, glial maturation factor, beta, which causes differentiation of brain cells, and inhibits proliferation.Envelope incorporation was not altered by modulation of the ratio of transfected DNA. The discrepancy in envelope incorporation between signature and non-signature pseudovirions was similar at both transfection ratios. This was true for both signature and non-signature pseudovirions. These results suggest that envelopes with the position 12 signature were incorporated at higher density into virions. Recent case series or studies reported an association of D313Y with other typical FD manifestations, e.g. peripheral neuropathy, hypertrophic cardiomyopathy, renal failure, or stroke. However, most authors considered the D313Y mutation as non-causal. Thus, as a consequence, to date almost all D313Ycarriers are not treated with ERT. Other studies support our results and found also primarily neurological organ manifestations in patients carrying GLA D313Y. In this respect, a recent prospective study including 625 patients with cerebralis chemia aged between18 and 55 reported that GLA D313Y was associated with cryptogenic stroke. Recent reports point to an association of particular mutations with a “late-onset” or “intermediate” type of FD, e.g. N215S, A143T or F113C. In this regard, the authors concluded thatmutations thatwere formerly assumed as non-causal but nonetheless showed variable FD symptoms might be considered as “predisposing polymorphisms”. In view of the above mentioned studies, this could particularly be the case with the D313Y mutation causing a CNS involvement. It should, however, be noted that our findings could still represent a clinical coincidence. Thus, further studies are necessary to confirm a causal relationship between the D313Y mutation and cerebral manifestations.