Редактирование: APLP2 (раздел)

==Publications==

{{medline-entry
|title=Analysis of Motor Function in Amyloid Precursor-Like Protein 2 Knockout Mice: The Effects of Ageing and Sex.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/30362021
|abstract=The amyloid precursor protein ([[APP]]) is a member of a conserved gene family that includes the amyloid precursor-like proteins 1 (APLP1) and 2 ([[APLP2]]). [[APP]] and [[APLP2]] share a high degree of similarity, and have overlapping patterns of spatial and temporal expression in the central and peripheral tissues, in particular at the neuromuscular junction. [[APP]]-family knockout (KO) studies have helped elucidate aspects of function and functional redundancy amongst the [[APP]]-family members. In the present study, we investigated motor performance of [[APLP2]]-KO mice and the effect sex differences and age-related changes have on motor performance. [[APLP2]]-KO and WT (on C57Bl6 background) littermates control mice from 8 (young adulthood) to 48 weeks (middle age) were investigated. Analysis of motor neuron and muscle morphology showed [[APLP2]]-KO females but not males, had less age-related motor function impairments. We observed age and sex differences in both motor neuron number and muscle fiber size distribution for [[APLP2]]-KO mice compared to WT (C57Bl6). These alterations in the motor neuron number and muscle fiber distribution pattern may explain why female [[APLP2]]-KO mice have far better motor function behaviour during ageing.
|mesh-terms=* Age Factors
* Aging
* Amyloid beta-Protein Precursor
* Animals
* Female
* Male
* Mice, Inbred C57BL
* Mice, Knockout
* Motor Activity
* Motor Neurons
* Muscle, Skeletal
* Sex Factors
* Spinal Cord
|keywords=* Ageing
* Amyloid precursor protein
* Amyloid precursor-like protein
* Knockout
* Motor neurons
* Sex differences
|full-text-url=https://sci-hub.do/10.1007/s11064-018-2669-6
}}
{{medline-entry
|title=Amyloid Precursor-Like Protein 2 deletion-induced retinal synaptopathy related to congenital stationary night blindness: structural, functional and molecular characteristics.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27267879
|abstract=Amyloid precursor protein knockout mice ([[APP]]-KO) have impaired differentiation of amacrine and horizontal cells. [[APP]] is part of a gene family and its paralogue amyloid precursor-like protein 2 ([[APLP2]]) has both shared as well as distinct expression patterns to [[APP]], including in the retina. Given the impact of [[APP]] in the retina we investigated how [[APLP2]] expression affected the retina using [[APLP2]] knockout mice ([[APLP2]]-KO). Using histology, morphometric analysis with noninvasive imaging technique and electron microscopy, we showed that [[APLP2]]-KO retina displayed abnormal formation of the outer synaptic layer, accompanied with greatly impaired photoreceptor ribbon synapses in adults. Moreover, [[APLP2]]-KO displayed a significant decease in ON-bipolar, rod bipolar and type 2 OFF-cone bipolar cells (36, 21 and 63 %, respectively). Reduction of the number of bipolar cells was accompanied with disrupted dendrites, reduced expression of metabotropic glutamate receptor 6 at the dendritic tips and alteration of axon terminals in the OFF laminae of the inner plexiform layer. In contrast, the [[APP]]-KO photoreceptor ribbon synapses and bipolar cells were intact. The [[APLP2]]-KO retina displayed numerous phenotypic similarities with the congenital stationary night blindness, a non-progressive retinal degeneration disease characterized by the loss of night vision. The pathological phenotypes in the [[APLP2]]-KO mouse correlated to altered transcription of genes involved in pre- and postsynatic structure/function, including [[CACNA1F]], [[GRM6]], TRMP1 and Gα0, and a normal scotopic a-wave electroretinogram amplitude, markedly reduced scotopic electroretinogram b-wave and modestly reduced photopic cone response. This confirmed the impaired function of the photoreceptor ribbon synapses and retinal bipolar cells, as is also observed in congenital stationary night blindness. Since congenital stationary night blindness present at birth, we extended our analysis to retinal differentiation and showed impaired differentiation of different bipolar cell subtypes and an altered temporal sequence of development from OFF to ON laminae in the inner plexiform layer. This was associated with the altered expression patterns of bipolar cell generation and differentiation factors, including MATH3, CHX10, [[VSX1]] and [[OTX2]]. These findings demonstrate that [[APLP2]] couples retina development and synaptic genes and present the first evidence that [[APLP2]] expression may be linked to synaptic disease.
|mesh-terms=* Aging
* Amacrine Cells
* Amyloid beta-Protein Precursor
* Animals
* Animals, Newborn
* Cell Differentiation
* Complement System Proteins
* Dendrites
* Eye Diseases, Hereditary
* Gene Deletion
* Genetic Diseases, X-Linked
* Mice, Inbred C57BL
* Mice, Knockout
* Myopia
* Neurogenesis
* Night Blindness
* Photoreceptor Cells, Vertebrate
* Presynaptic Terminals
* RNA, Messenger
* Retinal Bipolar Cells
* Synaptic Transmission
* Transcription Factors
* Transcription, Genetic
|keywords=* Amyloid precursor protein
* Amyloid precursor-like protein 2
* Congenital stationary night blindness
* Differentiation
* Synapses
* Synaptopathy
* Transcription
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4897877
}}
{{medline-entry
|title=Combined deletions of amyloid precursor protein and amyloid precursor-like protein 2 reveal different effects on mouse brain metal homeostasis.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/24448592
|abstract=Alterations to the expression of the Amyloid Precursor Protein ([[APP]]) and its paralogue Amyloid Precursor-Like Protein 2 ([[APLP2]]) affect metal homeostasis in vitro and in vivo. Analysis of the in vivo effects of the [[APP]] and [[APLP2]] knockouts on metal homeostasis has been restricted to [[APP]] and [[APLP2]] single knockout mice, and up to12 month old animals. To define the redundancy and inter-relationship between the [[APP]] and [[APLP2]] genes as regulators of metal homeostasis, and how this is influenced by aging, we investigated copper, iron, zinc and manganese levels in [[APP]] and [[APLP2]] single knockout mice as well as homozygous:hemizygous knockout mice at 3, 12 and 18 plus months of age. These studies identified age and genotype dependent changes in metal levels, and established differences in the relative roles played by [[APP]] and [[APLP2]] in modulating metal homeostasis. 
|mesh-terms=* Aging
* Alzheimer Disease
* Amyloid beta-Protein Precursor
* Animals
* Brain
* Copper
* Gene Deletion
* Homeostasis
* Iron
* Manganese
* Metals, Heavy
* Mice
* Mice, Inbred C57BL
* Mice, Knockout
* Zinc

|full-text-url=https://sci-hub.do/10.1039/c3mt00358b
}}