Human APP blocking peptide (CDBP0393)

Synthetic Human APP blocking peptide for BL, IHC

Product Overview
APP ( C - term ) peptide ( human )
Amyloid Precursor Protein
Species Reactivity
0.2 mg/ml
50 μg
PBS with 0.1% BSA 0.02% sodium azide pH7.2
0.02% Sodium Azide
Upon receipt - Keep as concentrated solution. Aliquot and store at -20℃ or below. Avoid freeze-thaw cycles.
UniProt ID
Antigen Description
This gene encodes a cell surface receptor and transmembrane precursor protein that is cleaved by secretases to form a number of peptides. Some of these peptides are secreted and can bind to the acetyltransferase complex APBB1/TIP60 to promote transcriptional activation, while others form the protein basis of the amyloid plaques found in the brains of patients with Alzheimer disease. Mutations in this gene have been implicated in autosomal dominant Alzheimer disease and cerebroarterial amyloidosis (cerebral amyloid angiopathy). Multiple transcript variants encoding several different isoforms have been found for this gene. [provided by RefSeq, Jul 2008]
DNA binding; PTB domain binding; acetylcholine receptor binding; growth factor receptor binding; heparin binding; identical protein binding; peptidase activator activity; protein binding; receptor binding; serine-type endopeptidase inhibitor activity; tra
APP; amyloid beta (A4) precursor protein; AAA; AD1; PN2; ABPP; APPI; CVAP; ABETA; PN-II; CTFgamma; amyloid beta A4 protein; preA4; protease nexin-II; peptidase nexin-II; beta-amyloid peptide; alzheimer disease amyloid protein; cerebral vascular amyloid peptide;


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Histological changes in thalamus in short term survivors following traumatic brain injury: An autopsy study


Authors: Bisht, Ajay; Garg, Kanwaljeet; Agarwal, Deepak; Singh, Pankaj Kumar; Satyarthee, Guru Dutt; Gupta, Deepak; Sinha, Sumit; Kakkar, Aanchal; Suri, Vaishali; Lalwani, Sanjeev; Kale, Shashank Sarad; Sharma, Bhawani Shankar

Background: Severe traumatic brain injury (TBI) is a major cause of morbidity and mortality. Reduction of thalamic volumes were seen in upto 80% of patients who survived for more than 3 months after TBI. However, the same may not be true in patients who died earlier following TBI. Aims: To to study the thalamus for evidence of any injury in short term survivors of TBI (<5 days) using immunohistochemistry to look for evidence of acute thalamic injury. Materials and Methods: A cross sectional prospective study was done in which autopsy specimens of short term survivors of TBI (<5 days) were studied for histopathological changes. Results: A total of 16 patients with a mean age of 37.8 years were included in the study. CT scan revealed acute subdural haematoma in 10, contusions in 4 patients, extradural haematoma and depressed fracture in 1 each, and diffuse axonal injury in 1 patient. Seven patients required surgery in the form of a decompressive hemicraniectomy. The histopathological analysis of the bilateral thalami showed evidence of congestion of the cerebral capillaries in 8 patients. Axonal retraction balls were seen in 8 patients, myelin breakdown products were seen in 14 patients and axonal swelling was seen in 14 patients. Conclusions: Thalamic injury is universal in the setting of severe TBI in patients who have decreased survival and may be a significant factor for the poor outcome in these patients.

Retinal amyloid peptides and complement factor H in transgenic models of Alzheimer's disease


Authors: Alexandrov, Peter N.; Pogue, Aileen; Bhattacharjee, Surjyadipta; Lukiw, Walter J.

Murine transgenic models of Alzheimer's disease (Tg-AD) have been useful to analyze the contribution of beta-amyloid precursor protein (beta APP), A beta 42 peptide deposition, and the proinflammatory mechanisms that characterize Alzheimer-type neuropathology. In this report, we have studied the levels of beta APP, A beta 40 and A beta 42 peptide, as well as the innate immune and inflammatory response-regulator complement factor H in the brain and retina in four different Tg-AD models including Tg2576, PSAPP, 3xTg-AD, and 5xFAD. Aged, symptomatic 5xFAD mice showed the highest retinal abundance of A beta 42 peptides and the highest deficits in complement factor H. This may be a useful model to study the mechanisms of amyloid-mediated inflammatory degeneration. The superior colliculus and retina obtained from late-stage Alzheimer's disease revealed upregulated amyloidogenic and inflammatory signaling along the anteroposterior axis of the retinal-primary visual cortex pathway. NeuroReport 22:623-627 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.

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