PRUNE and NM23-M1 expression in embryonic and adult mouse brain

被引:27
作者
Carotenuto, Pietro
Marino, Natascia
Bello, Anna Maria
D'Angelo, Anna
Di Porzio, Umberto
Lombardi, Daniela
Zollo, Massimo
机构
[1] Univ Naples Federico II, Dipartimento Biochim & Biotecnol Med, Naples, Italy
[2] CNR, Inst Genet & Biophys Adriano Buzzati, IGB, Naples, Italy
[3] CEINGE, Biotecnol Avanzate Scarl, I-80145 Naples, Italy
[4] Univ Aquila, Dept Expt Med, I-67100 Laquila, Italy
关键词
PDE; cAMP; NDPK; neurogenesis; differentiation; proliferation; nrain development; PRUNE; NM23;
D O I
10.1007/s10863-006-9044-z
中图分类号
Q6 [生物物理学];
学科分类号
071011 ;
摘要
A genetic interaction between PRUNE and NM23/NDPK has been postulated in Drosophila melanogaster. Many have focused on Drosophila for the genetic combination between PRUNE "knock down" and AWD/NM23 fly mutants bearing the P97S mutation (K-pn, Killer of PRUNE mutation). We postulated a role for PRUNE-NM23 interactions in vertebrate development, demonstrating a physical interaction between the human PRUNE and NM23-H1 proteins, and partially characterizing their functional significance in cancer progression. Here, we present an initial analysis towards the functional characterization of the PRUNE-NM23 interaction during mammalian embryogenesis. Our working hypothesis is that PRUNE, NM23-H1 and their protein-protein interaction partners have important roles in mammalian brain development and adult brain function. Detailed expression analyses from early mouse brain development to adulthood show significant co-expression of these two genes during embryonic stages of brain development, especially focusing on the cortex, hippocampus, midbrain and cerebellum. We hypothesize that their abnormal expression results in an altered pathway of activation, influencing protein complex formation and its protein partner interactions in early embryogenesis. In the adult brain, their function appears concentrated towards their enzyme activities, wherein biochemical variations can result in brain dysfunction.
引用
收藏
页码:233 / 246
页数:14
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