Mouse Amyloid beta A4 protein(APP) ELISA kit

Instructions
Code CSB-EL001950MO
Size 96T,5×96T,10×96T
See More Details 24T ELISA kits trial application
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Product Details

Target Name amyloid beta (A4) precursor protein
Alternative Names AppAmyloid-beta A4 protein ELISA Kit; ABPP ELISA Kit; APP ELISA Kit; Alzheimer disease amyloid A4 protein homolog ELISA Kit; Amyloid precursor protein ELISA Kit; Amyloid-beta precursor protein ELISA Kit; Amyloidogenic glycoprotein ELISA Kit; AG) [Cleaved into: N-APP; Soluble APP-alpha ELISA Kit; S-APP-alpha); Soluble APP-beta ELISA Kit; S-APP-beta); C99 ELISA Kit; APP-C99 ELISA Kit; Beta-secretase C-terminal fragment ELISA Kit; Beta-CTF); Amyloid-beta protein 42 ELISA Kit; Abeta42 ELISA Kit; Beta-APP42); Amyloid-beta protein 40 ELISA Kit; Abeta40 ELISA Kit; Beta-APP40); C83 ELISA Kit; Alpha-secretase C-terminal fragment ELISA Kit; Alpha-CTF); P3(42); P3(40); C80; Gamma-secretase C-terminal fragment 59 ELISA Kit; APP-C59 ELISA Kit; Amyloid intracellular domain 59 ELISA Kit; AID(59) ELISA Kit; Gamma-CTF(59)); Gamma-secretase C-terminal fragment 57 ELISA Kit; APP-C57 ELISA Kit; Amyloid intracellular domain 57 ELISA Kit; AID(57) ELISA Kit; Gamma-CTF(57)); Gamma-secretase C-terminal fragment 50 ELISA Kit; Amyloid intracellular domain 50 ELISA Kit; AID(50) ELISA Kit; Gamma-CTF(50)); C31] ELISA Kit
Abbreviation APP
Uniprot No. P12023
Species Mus musculus (Mouse)
Sample Types serum, plasma, tissue homogenates
Detection Range 15.6 ng/mL-1000 ng/mL
Sensitivity 3.9 ng/mL
Assay Time 1-5h
Sample Volume 50-100ul
Detection Wavelength 450 nm
Research Area Neuroscience
Assay Principle quantitative
Measurement Sandwich
Precision
Intra-assay Precision (Precision within an assay): CV%<8%
Three samples of known concentration were tested twenty times on one plate to assess.
Inter-assay Precision (Precision between assays): CV%<10%
Three samples of known concentration were tested in twenty assays to assess.
Linearity
To assess the linearity of the assay, samples were spiked with high concentrations of mouse APP in various matrices and diluted with the Sample Diluent to produce samples with values within the dynamic range of the assay.
  Sample Serum(n=4)
1:1 Average % 87
Range % 84-92
1:2 Average % 102
Range % 96-107
1:4 Average % 93
Range % 88-97
1:8 Average % 95
Range % 89-99
Recovery
The recovery of mouse APP spiked to levels throughout the range of the assay in various matrices was evaluated. Samples were diluted prior to assay as directed in the Sample Preparation section.
Sample Type Average % Recovery Range
Serum (n=5) 97 93-101
EDTA plasma (n=4) 102 92-105
Typical Data
These standard curves are provided for demonstration only. A standard curve should be generated for each set of samples assayed.
ng/ml OD1 OD2 Average Corrected
1000 2.213 2.342 2.278 2.160
500 1.586 1.665 1.626 1.508
250 1.060 1.097 1.079 0.961
125 0.673 0.683 0.678 0.560
62.5 0.407 0.412 0.410 0.292
31.2 0.281 0.294 0.288 0.170
15.6 0.195 0.200 0.198 0.080
0 0.117 0.118 0.118  
Troubleshooting
and FAQs
ELISA kit FAQs
Storage Store at 2-8°C. Please refer to protocol.
Lead Time 5-7 working days

Target Data

Function Functions as a cell surface receptor and performs physiological functions on the surface of neurons relevant to neurite growth, neuronal adhesion and axonogenesis. Involved in cell mobility and transcription regulation through protein-protein interactions. Can promote transcription activation through binding to APBB1-KAT5 and inhibit Notch signaling through interaction with Numb. Couples to apoptosis-inducing pathways such as those mediated by G(O) and JIP. Inhibits G(o) alpha ATPase activity (By similarity). Acts as a kinesin I membrane receptor, mediating the axonal transport of beta-secretase and presenilin 1. May be involved in copper homeostasis/oxidative stress through copper ion reduction. Can regulate neurite outgrowth through binding to components of the extracellular matrix such as heparin and collagen I and IV (By similarity). The splice isoforms that contain the BPTI domain possess protease inhibitor activity. Induces a AGER-dependent pathway that involves activation of p38 MAPK, resulting in internalization of amyloid-beta peptide and leading to mitochondrial dysfunction in cultured cortical neurons (By similarity). Provides Cu(2+) ions for GPC1 which are required for release of nitric oxide (NO) and subsequent degradation of the heparan sulfate chains on GPC1.
Gene References into Functions
  1. This study uncovered two clear phases in the life of APP23 mice: developmental and aging. Development displays similarities to young carriers of familial Alzheimer's disease (AD) mutations. All gene expression differences between APP23 and control mice correlate with aging. Age-related expression changes appear exacerbated/accelerated in APP23 mice. PMID: 27838490
  2. These results provide evidence for an emerging role of BAG-1M in the regulation of BACE1 expression and AD pathogenesis and that targeting the BAG-1M-NF-kappaB complex may provide a mechanism for inhibiting Abeta production and plaque formation. PMID: 28502705
  3. Conformational changes in a mouse model of Alzheimer's disease-linked amyloid beta and APP take place before the amyloids plaques can be seen. PMID: 28287086
  4. These results support the proposition that Aβ release during thrombosis serves as part of a natural defense against infection. PMID: 29890636
  5. These data suggest a novel regulatory function of juxta- and intra-membrane domains on the metabolism and function of APP. PMID: 29777707
  6. Inflammasome-derived cytokine IL18 suppresses amyloid-induced seizures in Alzheimer-prone mice. PMID: 30127003
  7. pharmacological inhibition of PARP-1 reversed both particulate matter-induced Abeta increase and glial activation. PMID: 29654761
  8. The concentrations of Abeta (1-42) were also significantly higher in early stage Alzheimer's disease (AD) mice compared with WT mice, however, the levels were markedly lower compared with later stage AD mice, as determined by ELISA. In addition to increased levels of Abeta (1-42) in mice with later stage AD, reduced astrocyte staining was observed compared with WT mice. PMID: 29568933
  9. work expands the current knowledge regarding Abeta seeding and the consequences thereof and attributes microglia an important role in diminishing Abeta seeding by environmental enrichment. PMID: 29229786
  10. This study demonstrated that APP as a novel receptor for Slit ligand mediating axon guidance and neural circuit formation. PMID: 28785723
  11. In vivo, the NHE6 knockout (NHE6(KO)) mouse model showed elevated Abeta in the brain, consistent with a causal effect. Increased nuclear translocation of histone deacetylase 4 (HDAC4) in ApoE4 astrocytes, compared with the nonpathogenic ApoE3 allele, suggested a mechanistic basis for transcriptional down-regulation of NHE6. PMID: 29946028
  12. This commentary reviews the role of the Alzheimer amyloid peptide Abeta on basal synaptic transmission, synaptic short-term plasticity, as well as short- and long-term potentiation in transgenic mice, with a special focus on N-terminal truncated Abeta4-42. PMID: 29561816
  13. ADAP KO mice developed glomerular pathology. ADAP KO podocytes lack cell protrusions with actin cytoskeleton forming circumferential stress fibers. PMID: 29192064
  14. Therefore, APP modulates Nav1.6 sodium channels through a Go-coupled JNK pathway, which is dependent on phosphorylation of APP at Thr668. PMID: 28008944
  15. These findings suggest that in the absence of CLU, Abeta clearance shifts to perivascular drainage pathways, resulting in fewer parenchymal plaques but more CAA because of loss of CLU chaperone activity, complicating the potential therapeutic targeting of CLU for AD. PMID: 28701379
  16. Chronic Dyrk1 inhibition reversed cognitive deficits in Alzheimer's disease transgenic mice via reduction of APP and phosphorylated tau pathology. PMID: 28779511
  17. The findings provide a model for initiation of synaptic dysfunction whereby exposure to physiologic levels of amyloid beta for a prolonged period of time causes microstructural changes at the synapse which result in increased transmitter release, failure of synaptic plasticity, and memory loss. PMID: 27581852
  18. The results of the present study substantiate that cGMP has a role in the endocytic pathway of APP and suggest a scenario where the cyclic nucleotide enhances the production of Abeta by favoring the trafficking of APP from the cell cortex to the endolysosomal compartment. PMID: 28789837
  19. Study showed that the APP Osaka mutation has dual effects: it causes a loss-of-function of APP and gain-of-toxic-function of Abeta, though the latter seems to come out only after the former causes GABAergic depletion. Also present OSK-KI mice as a mouse model to replicate the hereditary form of recessive familial Alzheimer's disease. PMID: 28760161
  20. Enhancing mitochondrial proteostasis reduces amyloid-beta proteotoxicity PMID: 29211722
  21. Results show that the duration of UP state, which is a key feature of cortical synaptic integration occurring predominantly during slow-wave sleep, is significantly increased in the prefrontal cortex in the absence of APP. This was accompanied by a specific reduction in the glutamine synthetase and tissue GABA content and sequential upregulation in the levels of GABA-B receptor expression. PMID: 27552836
  22. results support the hypothesis that the miR-132/212 network, including Sirt1 and likely other target genes, contributes to abnormal Abeta metabolism and senile plaque deposition in AD. PMID: 27484949
  23. Activation of CaMKIV by soluble amyloid-beta1-42 impedes trafficking of axonal vesicles and impairs activity-dependent synaptogenesis PMID: 28698220
  24. Abpp /KPI(R13I) mutant mice were similarly deficient as Abpp knock out mice in regulating cerebral thrombosis in experimental models of carotid artery thrombosis and intracerebral hemorrhage. PMID: 28499154
  25. The cognitive function of APP/PS1 mice was impaired at 10months of age; moreover, the hypermetabolic state identified in various brain regions at 5months of age was also significantly decreased. PMID: 29107091
  26. APP heterozygosity results in greater decreases of cortical APP in Transgenic (Tg) versus non-Tg mice. Mutant huntingtin transgenic mice develop brain iron accumulation as a result of greater suppression of APP levels. Elevated brain iron in Tg mice was associated with a decline in motor endurance consistent with a disease promoting effect of iron in the YAC128 model of human Huntington's Disease. PMID: 28550267
  27. Mass spectrometry analysis of APP intracellular domains revealed differential processing of APP-C83, APP-C89, and APP-C99 by gamma-secretase already at the epsilon-cleavage stage. This mechanistic insight could aid in developing substrate-targeted modulators of APP-C99 processing to specifically lower the Abeta42:Abeta40 ratio without compromising gamma-secretase function. PMID: 28591569
  28. Data show that exosomal amyloid precursor protein C-terminal fragments (APP-CTFs) and bis(monoacylglycero)phosphate (BMP) as candidate biomarkers diagnostic of endolysosomal dysfunction associated with neurodegenerative disorders. PMID: 29348617
  29. study provides molecular insights into the design of amyloidogenic inhibitors to cure various neurodegenerative and amyloid-associated diseases, as NABi would regulate aggregation of other toxic beta-sheet proteins other than Abeta. PMID: 29107146
  30. Conducted in vivo extracellular recording to investigate cholinergic compound action potentials of the superior cervical ganglion (SCG) in APP(-/-) and littermate wild-type (WT) mice; found that APP not only regulates presynaptic activity, but also affects postsynaptic function at cholinergic synapses in SCG; also alpha4beta2 and alpha7 nicotinic acetylcholine receptors are reduced in the absence of APP. PMID: 27553120
  31. App-KI mouse lines with different levels of pathophysiology are useful models of AD. PMID: 27377630
  32. Loss of Abpp is associated with cognitive impairment. PMID: 27049828
  33. long term survival and amyloid protein levels are modified by positive and negative early life experiences in a mouse model of Alzheimer's disease PMID: 27259247
  34. the synaptic localization of APP, ADAM10, and BACE1 in the mouse cerebral cortex, was examined. PMID: 26497029
  35. Taken together, these results suggest that apoE-containing discoidal HDLs do not require LCAT-dependent maturation to mediate efficient Abeta clearance PMID: 24950691
  36. APP knockout mice have shorter dendritic arbors in the hippocampus. PMID: 27664851
  37. This study demonstrates the neuroprotective effect of TSG on APP expression, suggesting that TSG may be beneficial for AD prevention and treatment. PMID: 29129695
  38. SNX15 regulates the recycling of APP to cell surface and, thus, its processing for Abeta generation. PMID: 26115702
  39. Immunohistochemical analysis confirmed increased amount of NOS1 protein in neuronal somata and processes in the perilesional cortex in APP/PS1-severe traumatic brain injury(TBI) mice compared to APP/PS1-sham (p < 0.05) or Wt-sTBI mice (p < 0.01). PMID: 26671618
  40. Combining a murine APP-deficient and a human APP-transgenic strain, we were able to analyse the progression of the cortical amyloidosis independent of the murine variant. The lack of endogenous mAPP resulted in accelerated deposition and, thus, increased number of senile plaques and higher levels of aggregated hAbeta. PMID: 28637503
  41. our findings indicate that sortilin is a beneficial protein for the reduction of amyloid pathology in APP/PS1 mice by promoting APP degradation PMID: 29056359
  42. APP levels then decrease progressively as a function of age in close relationship with the gradual normalization of FMRP and hnRNP C levels. PMID: 26048669
  43. a 99-aa C-terminal fragment of APP,C99, in addition to its localization in endosomes, can also be found in mitochondria-associated endoplasmic reticulum (ER) membranes, where it is normally processed rapidly by gamma-secretase. PMID: 29018038
  44. The authors concluded that the FcgammaRIIb-SHIP2 axis links Abeta neurotoxicity to tau pathology by dysregulating phosphoinositide metabolism, providing insight into therapeutic potential against Alzheimer's disease. PMID: 27834631
  45. results suggest that PrP(C) recognizes structural features common to both Abeta oligomers and fibril ends and that this interaction could contribute to the neurotoxic effect of Abeta aggregates. PMID: 28842494
  46. Our study provides the first direct evidence that Abeta, an AD-linked factor, is associated to the pathogenesis of ALS and provides molecular clues to understand common aggregation mechanisms in the pathogenesis of neurodegenerative diseases. PMID: 28864422
  47. These data provide evidence that amyloid beta acts to enhance tau pathology by increasing the formation of tau species capable of seeding new aggregates. PMID: 28500862
  48. Although hyperactivity and hypersynchronicity were respectively detected in mice expressing the PS2-N141I or the APP Swedish mutant alone, the increase in cross-frequency coupling specifically characterized the 6-month-old PS2APP mice, just before the surge of the cognitive decline PMID: 27889678
  49. these results uncover a novel role for mDia1 in Abeta-mediated synaptotoxicity and demonstrate that inhibition of MT dynamics and accumulation of PTMs are driving factors for the induction of tau-mediated neuronal damage. PMID: 28877993
  50. APP and its metabolites are capable of influencing the basic physiology of the pancreas. PMID: 28710249
  51. treatment of APP/E4/Abca1+/- mice with liver X receptor (LXR) agonist T0 ameliorates APOE4-induced Alzheimer's disease (AD)-like pathology and therefore targeting the LXR-ABCA1-APOE regulatory axis could be effective as a potential therapeutic approach in AD patients, carriers of APOEepsilon4 PMID: 28241068
  52. These results provide evidence supporting a key role for the p38 MAPK signaling pathway which is involved in the regulation of Abeta1-42 internalization in the parietal cortex and hippocampus of mouse through LRP1 in vivo. PMID: 27163530
  53. increased APP and/or beta-CTF impact the endocytic pathway to disrupt NGF trafficking and signaling, resulting in trophic deficits in basal forebrain cholinergic neurons. PMID: 27064279
  54. ABETA 25-35 downregulated miR-137 and upregulated TNFAIP1 in cortical neurons and N2a cells. PMID: 28655611
  55. These results indicate that platelet APP limits venous thromboembolism through a negative regulation of both fibrin formation and neutrophil function. PMID: 28611024
  56. These findings highlight for the first time that APP-dependent glial cell line-derived neurotropic factor expression drives the process of neuromuscular junction formation, providing new insights into the link between APP gene regulatory network and physiologic functions. PMID: 26718890
  57. The present findings confirm that high fat diet favors the formation of betaA depositions in the brain, a key feature of Alzheimer's disease, supporting the metabolic hypothesis of sporadic Alzheimer's disease. PMID: 27863851
  58. TREM2 protects from Alzheimer's disease by enabling microglia to surround and alter Abeta plaque structure, thereby limiting neuritic damage. PMID: 27091843
  59. To conclude, our data corroborate a major role of APP for structural plasticity and adaptive remodeling of cortical synapses in the adult brain. They also indicate that lack of APP holoprotein leads to impaired D-serine homeostasis, which is associated with dysfunctional synaptic plasticity. PMID: 27572463
  60. Pretreatment with a P-glycoprotein inhibitor, which blocks blood-brain barrier transport of Abeta, resulted in significant prolongation of Abeta40 half-life, but only in the latter phase of Abeta clearance from the interstitial fluid. PMID: 27069115
  61. in Alzheimer's disease (AD) brains, elevated DAPK1 levels showed co-relation with the increase of APP phosphorylation. Combined together, these results suggest that DAPK1 promotes the phosphorylation and amyloidogenic processing of APP, and that may serve a potential therapeutic target for AD. PMID: 27094130
  62. The Amyloid Precursor Protein contributes to calcium homeostasis in situations of metabolic stress. This finding may shed light on the physiological function of APP and may be important for understanding mechanisms of neurodegenerative diseases. PMID: 27511009
  63. The levels of MTERF4 protein were significantly increased in the hippocampus of APP/PS1 mice, an animal model of Alzheimer's disease. PMID: 27894840
  64. The results indicate that Nrx2alpha and NL1 are targets of Abeta oligomers and that prevention of this interaction reduces the deleterious impact of Abeta oligomers on synapses and cognition. PMID: 28283575
  65. These results support a role for APP in cortical lamination and demonstrate the utility of a conditional knockout approach in which APP can be deleted with temporal control in vivo. PMID: 28284905
  66. NGF signalling directly controls basal APP phosphorylation, subcellular localization and BACE cleavage. PMID: 27076121
  67. Therefore, SORL1 activation by 6-shogaol provides neuronal cell survival through the inhibition of Abeta production. These results indicate that 6-shogaol should be regarded as an SORL1 activator and a potential preventive agent for the treatment of AD. PMID: 28188785
  68. Abeta monomers physiologically favor Tau activity and dendritic sprouting, whereas their excess causes Tau pathology PMID: 27406053
  69. analysis suggests that some familial Alzheimer's disease mutations in APP are amyloidogenic and/or amyloidolytic via selection of alternative BACE1 cleavage sites PMID: 27687728
  70. results suggest that COX activity and amyloid deposition in brain are likely independent processes. PMID: 27425247
  71. Ln-gamma1 promotes internalization of PrPC and mGluR5 and transiently decreases AbetaO biding to neurons; however, the peptide does not impact AbetaO toxicity. Given that mGluR5 is critical for toxic signaling by AbetaOs and in prion diseases, we tested whether mGlur5 knock-out mice would be susceptible to prion infection. PMID: 27563063
  72. prion protein-derived cell-penetrating peptide cytotoxicity is modulated by pH but independent of amyloid formation PMID: 27818203
  73. This study further distinguishes two separate Abetao-dependent signaling cascades, one dependent on extracellular Ca(2+) and Fyn kinase activation and the other dependent on the release of Ca(2+) from intracellular stores. Thus, Abetao triggers multiple distinct PrP(C)-mGluR5-dependent events implicated in neurodegeneration and dementia. PMID: 27325698
  74. APP shares essential functions with APP-like protein-2 (APLP2) but not APP-like protein-1 (APLP1). Noteworthy, APLP2, but not APLP1, interacts with Stub1 and CRL4(CRBN), pointing to a functional pathway shared only by APP and APLP2. PMID: 27325702
  75. Orthopedic surgery induces Abeta accumulation and tau phosphorylation in the hippocampus. PMID: 27599409
  76. Results indicate that isomerization of Asp7 and phosphorylation of Ser8 of the amyloid beta peptide (Abeta) backbone have a significant impact on the profiles of brain Abeta binding proteins. PMID: 27400251
  77. Cadmium induces cell death on cholinergic neurons through blockade of M1 receptor, overexpression of AChE-S and GSK-3beta, down-regulation of AChE-R and increase in Abeta and total and phosphorylated tau protein levels. PMID: 26026611
  78. plasma Abeta(1-42) concentration increases with age, while the concentration of Abeta(1-42) in the cerebrospinal fluid (CSF) decreases in APPswe, PS1M146V and TauP301L transgenic (3xTg-AD) mice. PMID: 26830653
  79. The production of IFNgamma finally accelerated the deposition of Abeta1-42 in beta-amyloid plaques. PMID: 26869183
  80. A cell-permeable tool for analysing APP intracellular domain function and manipulation of PIKfyve activity. PMID: 26934981
  81. APP, tau, and synaptophysin were elevated in in the medial preoptic area in both the B6D2F1 and BXB1 maters relative to the B6D2F1 and BXB1 non-maters,suggesting a potential genetic mechanism for inheritance of steroid-independent male sexual behavior. PMID: 26940434
  82. amyloid-beta and tau expression in the brains of TgSwDI mice are attenuated by extra-virgin olive oil PMID: 26344778
  83. folic acid deficiency can enhance Abeta accumulation in APP/PS1 mice brain and decrease amyloid-associated miRNAs expression PMID: 26345540
  84. These data support the notion that APP and APLP2 facilitate transmitter release, likely through the interaction with the neurotransmitter release machinery. PMID: 26551565
  85. EphB2 prevents amyloid-beta-induced depletion of cell surface GluN1 requiring the PDZ-binding motif of EphB2. PMID: 26589795
  86. Data suggest that amyloid-beta (here, Abeta 1-42) induces acute and chronic synaptic dysfunction in part through inhibition of Eg5 (kinesin-5) in hippocampal neurons. PMID: 26957206
  87. the absence of Mt3 reduces Abeta uptake in astrocytes through an abnormality in actin polymerization. PMID: 26637294
  88. Mutant SOD1 Increases APP Expression and Phosphorylation in Cellular and Animal Models of ALS PMID: 26600047
  89. lactate levels remained elevated with age and increased aerobic glycolysis enzyme expression correlated with poorer memory performance in APP/PS1 mice PMID: 26865611
  90. young mouse WT splenocytes not only prevented AD, but also improved the spatial learning and memory of APPswe/PSENldE9 transgenic mice PMID: 26317549
  91. p38alpha MAPK plays a critical role in the regulation of BACE1 degradation and Abeta generation in Alzheimer Disease pathogenesis PMID: 26663083
  92. Swedish mutant APP-based BACE1 binding site peptide reduces APP beta-cleavage and cerebral Abeta levels in Alzheimer's mice. PMID: 26091071
  93. APP full length protein and/or its cleaved products are necessary to mount a complete and effective innate immune cell response to inflammatory injury. PMID: 26447481
  94. The study demonstrate that murine Abeta peptides have the capacity to produce amyloid deposits that are morphologically similar to deposits found in human AD provided the murine APP gene. PMID: 26566997
  95. Abeta oligomers in the cerebrospinal fluid (CSF) further promoted the expression of APH-1alpha/-1beta (by >2.5-fold), which enhances the gamma-cleavage of APP and Abeta deposition during AD progression PMID: 26293690
  96. Redox-mediated posttranslational modification of brain proteins link Abeta and hyperglycaemia to cognitive dysfunction in metabolic syndrome/type 2 diabetes and Alzheimer disease. PMID: 26743041
  97. Abeta was accumulated more in the ERalpha knockout mice brain and greatly worsened memory impairment and glial activation as well as neurogenic inflammation. PMID: 25128029
  98. Data indicate that body weight gain, high hepatic triglyceride, and hyperglycemia were positively associated with serum beta-amyloid. PMID: 26244977
  99. Findings indicate the physiological importance of Reelin in protecting the brain against amyloid beta (Abeta)-induced synaptic dysfunction and memory impairment. PMID: 26152694
  100. Reveal novel roles for APP in regulating neuromuscular synapse formation through hetero-oligomeric interaction with LRP4 and agrin and thereby provide new insights into the molecular mechanisms that govern NMJ formation and maintenance. PMID: 23986861

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Subcellular Location Membrane, Single-pass type I membrane protein, Membrane, clathrin-coated pit
Protein Families APP family
Tissue Specificity Isoform APP770 is expressed in kidney. Isoform APP751 is widely expressed. Isoform APP695 is expressed in brain, kidney and liver. Isoform APP695, isoform APP714 and isoform APP751 are expressed in several different brain regions including hippocampus, su
Database Links

KEGG: mmu:11820

STRING: 10090.ENSMUSP00000005406

UniGene: Mm.277585

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