Редактирование: APLP1

Amyloid-like protein 1 precursor (APLP) (APLP-1) [Contains: C30]

==Publications==

{{medline-entry
|title=Immunohistochemical and in situ analysis of amyloid precursor-like protein-1 and amyloid precursor-like protein-2 expression in Alzheimer disease and aged control brains.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/9729270
|abstract=Amyloid precursor protein ([[APP]]) is a ubiquitously expressed membrane spanning glycoprotein which is endoproteolytically processed to Abeta, a 39-43 amino acid peptide that is the main component of senile plaques in Alzheimer Disease (AD). [[APP]] is a member of a highly conserved gene family, including Amyloid Precursor-Like Proteins (APLPs) [[APLP1]] and [[APLP2]]. We now characterize [[APLP1]] and [[APLP2]] mRNA and protein expression in AD and aged control brains. Using in situ hybridization in hippocampal tissue from control and AD brain, we show that [[APLP1]] and [[APLP2]] mRNA are expressed primarily in the granule cells of the dentate gyrus, in areas [[CA1]]-[[CA3]], and subiculum. Immunohistochemistry reveals staining for both [[APLP1]] and [[APLP2]] in neurons and blood vessels in AD and control cases. In addition, in AD brain, large dystrophic neurites in a subset of senile plaques are conspicuously labeled with [[APLP1]] and [[APLP2]] antibodies. The aged control brains have significantly fewer immunoreactive plaques and dystrophic neurites. The regional, cellular, and subcellular distribution of [[APLP1]] and [[APLP2]] overlap with each other and with [[APP]]. These observations support the hypothesis that the members of this family of proteins may perform similar functions.
|mesh-terms=* Aged
* Aged, 80 and over
* Aging
* Alzheimer Disease
* Amyloid beta-Protein Precursor
* Cadaver
* Humans
* Immunohistochemistry
* In Situ Hybridization
* Nerve Tissue Proteins

|full-text-url=https://sci-hub.do/10.1016/s0006-8993(98)00653-2
}}
{{medline-entry
|title=Generation of [[APLP2]] KO mice and early postnatal lethality in [[APLP2]]/[[APP]] double KO mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/9461064
|abstract=Amyloid precursor protein ([[APP]]) is a member of a larger gene family including amyloid precursor-like proteins (APLP), [[APLP2]] and [[APLP1]]. To examine the function of [[APLP2]] in vivo, we generated [[APLP2]] knockout (KO) mice. They are of normal size, fertile, and appear healthy up to 22 months of age. We observed no impaired axonal outgrowth of olfactory sensory neurons following bulbectomy, suggesting against an important role for [[APLP2]] alone in this process. Because [[APLP2]] and [[APP]] are highly homologous and may serve similar functions in vivo, we generated mice with targeted [[APLP2]] and [[APP]] alleles. Approximately 80% of double KO mice die within the first week after birth, suggesting that [[APLP2]] and [[APP]] are required for early postnatal development. The surviving approximately 20% of double KO mice are 20-30% reduced in weight and show difficulty in righting, ataxia, spinning behavior, and a head tilt, suggesting a deficit in balance and/or strength. Adult double KO mice mate poorly, despite apparent normal ovarian and testicular development. Otherwise, double KO mice appear healthy up to 13 months of age. We conclude, that [[APLP2]] and [[APP]] can substitute for each other functionally.
|mesh-terms=* Amyloid beta-Protein Precursor
* Animals
* Animals, Newborn
* Ataxia
* Behavior, Animal
* Blastocyst
* Brain
* Gene Targeting
* Immunohistochemistry
* Life Expectancy
* Mice
* Mice, Knockout
* Nerve Regeneration
* Olfactory Bulb
* Postural Balance
* Sexual Behavior, Animal

|full-text-url=https://sci-hub.do/10.1016/s0197-4580(97)00151-6
}}