期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 110, 期 47, 页码 18952-18957出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1221172110
关键词
sciatic nerve; NGF; p53 family; CGRP
资金
- Medical Research Council (Leicester, UK)
- Alleanza contro il Cancro [ACC12-ACC6]
- Ministero Istruzione Universit a Ricerca/Progetti di Ricerca di Interesse Nazionale [RBIP06LCA9_0023]
- Associazione Italiana per la Ricerca sul Cancro [20082010_33-08]
- 5xmille [9979]
- Telethon Grant [GGPO9133]
- Ministero della Salute (Ricerca Oncologica) [26/07]
- IDI-IRCCS Grant [RF06]
- Medical Research Council [MC_U132670600, MC_U132681855] Funding Source: researchfish
- MRC [MC_U132670600, MC_U132681855] Funding Source: UKRI
Total and N-terminal isoform selective p73 knockout mice show a variety of central nervous system defects. Here we show that TAp73 is a transcriptional activator of p75 neurotrophin receptor (p75(NTR)) and that p75(NTR) mRNA and protein levels are strongly reduced in the central and peripheral nervous systems of p73 knockout mice. In parallel, primary cortical neurons from p73 knockout mice showed a reduction in neurite outgrowth and in nerve growth factor-mediated neuronal differentiation, together with reduced miniature excitatory postsynaptic current frequencies and behavioral defects. p73 null mice also have impairments in the peripheral nervous system with reduced thermal sensitivity, axon number, and myelin thickness. At least some of these morphological and functional impairments in p73 null cells can be rescued by p75(NTR) re-expression. Together, these data demonstrate that loss of p75(NTR) contributes to the neurological phenotype of p73 knockout mice.
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