DCC

Материал из hpluswiki
Перейти к навигации Перейти к поиску

Netrin receptor DCC precursor (Colorectal cancer suppressor) (Immunoglobulin superfamily DCC subclass member 1) (Tumor suppressor protein DCC) [IGDCC1]

Publications[править]

X Chromosome Domain Architecture Regulates Caenorhabditis elegans Lifespan but Not Dosage Compensation.


Dynamic functional connectivity analysis of functional MRI based on copula time-varying correlation.


Comprehensive outpatient rehabilitation increases the ability of people over 60 to live independently.

{{medline-entry |title=Mesocorticolimbic Connectivity and Volumetric Alterations in [i]DCC[/i] Mutation Carriers. |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29712788 |abstract=The axon guidance cue receptor DCC (deleted in colorectal cancer) plays a critical role in the organization of mesocorticolimbic pathways in rodents. To investigate whether this occurs in humans, we measured (1) anatomical connectivity between the substantia nigra/ventral tegmental area (SN/VTA) and forebrain targets, (2) striatal and cortical volumes, and (3) putatively associated traits and behaviors. To assess translatability, morphometric data were also collected in [i]Dcc[/i]-haploinsufficient mice. The human volunteers were 20 [i]DCC[/i] mutation carriers, 16 [i]DCC[/i] relatives, and 20 [i]DCC[/i] unrelated healthy volunteers (UHVs; 28 females). The mice were 11 [i]Dcc[/i] and 16 wild-type C57BL/6J animals assessed during adolescence and adulthood. Compared with both control groups, the human [i]DCC[/i] carriers exhibited the following: (1) reduced anatomical connectivity from the SN/VTA to the ventral striatum [[i]DCC[/i] : [i]p[/i] = 0.0005, [i]r[/i]([i]effect size[/i]) = 0.60; UHV: [i]p[/i] = 0.0029, [i]r[/i] = 0.48] and ventral medial prefrontal cortex ([i]DCC[/i] : [i]p[/i] = 0.0031, [i]r[/i] = 0.53; UHV: [i]p[/i] = 0.034, [i]r[/i] = 0.35); (2) lower novelty-seeking scores ([i]DCC[/i] : [i]p[/i] = 0.034, [i]d[/i] = 0.82; UHV: [i]p[/i] = 0.019, [i]d[/i] = 0.84); and (3) reduced striatal volume ([i]DCC[/i] : [i]p[/i] = 0.0009, [i]d[/i] = 1.37; UHV: [i]p[/i] = 0.0054, [i]d[/i] = 0.93). Striatal volumetric reductions were also present in [i]Dcc[/i] mice, and these were seen during adolescence ([i]p[/i] = 0.0058, [i]d[/i] = 1.09) and adulthood ([i]p[/i] = 0.003, [i]d[/i] = 1.26). Together these findings provide the first evidence in humans that an axon guidance gene is involved in the formation of mesocorticolimbic circuitry and related behavioral traits, providing mechanisms through which [i]DCC[/i] mutations might affect susceptibility to diverse neuropsychiatric disorders. Opportunities to study the effects of axon guidance molecules on human brain development have been rare. Here, the identification of a large four-generational family that carries a mutation to the axon guidance molecule receptor gene, [i]DCC[/i], enabled us to demonstrate effects on mesocorticolimbic anatomical connectivity, striatal volumes, and personality traits. Reductions in striatal volumes were replicated in [i]DCC[/i]-haploinsufficient mice. Together, these processes might influence mesocorticolimbic function and susceptibility to diverse neuropsychiatric disorders. |mesh-terms=* Adult

  • Aging
  • Animals
  • Axons
  • DCC Receptor
  • Exploratory Behavior
  • Female
  • Heterozygote
  • Humans
  • Limbic System
  • Magnetic Resonance Imaging
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Middle Aged
  • Neural Pathways
  • Personality Disorders
  • Prefrontal Cortex
  • Substance-Related Disorders
  • Substantia Nigra
  • Ventral Tegmental Area
  • Young Adult

|keywords=* axon guidance

  • brain morphometry
  • diffusion MRI
  • genetics
  • nicotine
  • personality

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5956985 }}

Dcc haploinsufficiency regulates dopamine receptor expression across postnatal lifespan.

{{medline-entry |title=Potential effect of mechano growth factor E-domain peptide on axonal guidance growth in primary cultured cortical neurons of rats. |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27863093 |abstract=Establishing appropriate synaptic connections and plasticity is a critical need in neuronal regeneration and development. Mechano growth factor (MGF) and its C-terminal E-domain peptide with 24 amino acids, MGF-Ct24E, are potential neuroprotective agents. Our preliminary study indicates that Netrin-1 can guide axonal growth and its expression is sensitive to MGF, but how MGF regulates the expression of Netrin-1 and its receptor DCC is still unclear. Here, we investigate the effect of MGF-Ct24E on the expression of Netrin-1 and DCC in primary cultured cortical neurons in vitro and the adult rat brain in vivo. MTT assay shows that MGF-Ct24E can significantly protect primary cortical neurons against nerve injury. There is a significant increase in axonal elongation after MGF-Ct24E treatment at concentrations of 0.5 and 1.0 μg/ml. Real-time polymerase chain reaction assay indicates that MGF-Ct24E can effectively promote the expression of Netrin-1 and DCC in primary cultured cortical neurons. To identify the certain mechanism of MGF-Ct24E on neuronal guidance and growth, adult rats are subjected to intramuscular injection of MGF-Ct24E after traumatic brain injury. Rats injected with MGF-Ct24E start eating and drinking within 14 days, indicating that MGF-Ct24E can promote rehabilitation. HE staining and immunohistochemistry assays of brain section slices reveal that MGF-Ct24E treatment can significantly inhibit the haemorrhage of traumatic brain injury and promote expression of Netrin-1. Further investigation of protein expression by Western blot assay shows that MGF-Ct24E promotes expression of Netrin-1 and DCC after nerve injury. MGF-Ct24E can effectively improve axonal guidance through upregulation of Netrin-1/DCC signalling in neuronal regeneration. Copyright © 2016 John Wiley