| Reactivity | HuSpecies Glossary |
| Applications | WB, IHC |
| Clonality | Polyclonal |
| Host | Goat |
| Conjugate | Unconjugated |
| Concentration | LYOPH |
| Immunogen | S. frugiperda insect ovarian cell line Sf 21-derived recombinant human APP 695+1 frameshift mutant Leu18-Arg336 Accession # NP_958817 |
| Specificity | Detects human APP695+1 and human APP770 in direct ELISAs and Western blots. This antibody recognizes a common epitope present on APP695+1 and APP770 found within the segments Leu18 - Arg288 or Pro365 - Arg411 of APP770 (Accession P05067). |
| Source | N/A |
| Isotype | IgG |
| Clonality | Polyclonal |
| Host | Goat |
| Gene | APP |
| Purity Statement | Antigen Affinity-purified |
| Innovator's Reward | Test in a species/application not listed above to receive a full credit towards a future purchase. |
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| Storage | Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
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| Buffer | Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. *Small pack size (SP) is supplied either lyophilized or as a 0.2 µm filtered solution in PBS. |
| Preservative | No Preservative |
| Concentration | LYOPH |
| Reconstitution Instructions | Reconstitute at 0.2 mg/mL in sterile PBS. |
Amyloid precursor protein (APP) is a type I membrane protein with several human isoforms due to alternative splicing. APP-770, -751, and -733 contain a Kunitz protease inhibitor (KPI) domain (residue 291 - 342) and APP-695 does not. APP is a cell surface molecule with many functions. It can be processed proteolytically in two different pathways. In one pathway, beta - and gamma -secretase cleave at the beta site between residue 670 and 671 and the gamma site between residue 711 and 714 to produce beta ‑amyloid peptide (A beta 40 and A beta 42), a major component in plaques found in brains of patients with Alzheimer's disease (1). The other pathway involves alpha -secretase that cleaves residues between 687 and 688. It is antiamyloidogenic due to its benign character and the prevention of the A beta peptide formation (2). Soluble APP containing the KPI domain, also referred to as protease nexin II, is a potent inhibitor of serine proteases and may have additional functions. For example, it may regulate the contact face of blood coagulation and limit thrombosis specially in brain due to its localization and coagulation factor XI inhibiting activity (3, 4).
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| Images | Ratings | Applications | Species | Date | Details | ||||||
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reviewed by:
Verified Customer |
IF | Mouse | 12/19/2014 |
Summary
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Secondary Antibodies |
Isotype Controls |
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HIV-associated neurocognitive disorders involve extracellular Nef-induced modification of lipid rafts and redistribution of Alzheimer’s disease-related proteins Jamshed Arslan, Pharm D, PhD Cholesterol is an essential part of animal cell membranes. Cholesterol-rich lipid rafts maintain the fluidity and protein trafficking of plasma membranes. Cellular ABCA1 protein moves cho... Read full blog post. |
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Mechanisms of Neurodegeneration: Protein aggregation and failure of autophagy By Michalina Hanzel, PhDIn a series of three blog posts I will briefly explore the major cellular mechanisms responsible for many neurodegenerative disorders. The first, and perhaps the most apparent, is the accumulat... Read full blog post. |
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Losing memory: Toxicity from mutant APP and amyloid beta explain the hippocampal neuronal damage in Alzheimer's disease By Jamshed Arslan Pharm.D. Alzheimer's disease (AD) is an irreversible brain disorder that destroys memory and thinking skills. The telltale signs of AD brains are extracellular deposits of amy... Read full blog post. |
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Lysosomal Dysfunction is Linked to Exosomal Secretion By Christina Towers, PhD. Lysosomal Dysfunction and DiseaseLysosomes are highly acidic organelles that are critical for cellular function and indispensable for degradative pathways like autophagy and endocytosis.... Read full blog post. |
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Immunity’s flipside: Microglia promote Alzheimer’s pathology during inflammation By Jamshed Arslan Pharm.D. Microglia are brain's macrophages. In Alzheimer's disease (AD), microglia clear up protein aggregates called amyloid beta plaques. The connection between immune activation and AD is unclea... Read full blog post. |
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The C99 fragment of amyloid precursor protein (APP) Alzheimer’s Disease (AD) is a neurodegenerative disorder that is characterized by an abundance of the beta-amyloid peptide in the brain. When AD was first discovered, it was determined that beta-amyloid was produced as a result of the prote... Read full blog post. |
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Beta Amyloid (MOAB2) and the link between traumatic brain injury and Alzheimer’s disease An epidemiological association between traumatic brain injury (TBI) and Alzheimer's disease (AD) has long been established. Interestingly, an increase in beta amyloid (one hallmark of AD) directly following TBI has been observed. In fact, it h... Read full blog post. |
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Niemann Pick-C1 and cholesterol dynamics Niemann-Pick type C1 (NPC1) mediates low-density cholesterol transport from late endosomes and lysosomes to other areas of the cell via receptor mediation endocytosis. Although cholesterol moves freely inside the cell, it cannot independently expo... Read full blog post. |
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FANCD2 and DNA damage repair Fanconi anemia (FA) is a genetically inherited disorder that yields cytogenetic instability, hypersensitivity to DNA crosslinking compounds and defective DNA repair. A variety of genes have been identified within the FA pathway that are referred t... Read full blog post. |
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Beta Amyloid Neurotoxicity and Alzheimer's Disease A major histopathological hallmark of Alzheimer's disease (AD) is the presence of amyloid deposits in the parenchyma of the amygdala, hippocampus, and neocortex. The principal component of amyloid is beta amyloid (AB). The pathologic accumulation of A... Read full blog post. |
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