beta Amyloid Polyclonal Antibody (CT695) | Invitrogen 51-2700 product information

product summary

company name :

Invitrogen

other brands :

NeoMarkers, Lab Vision, Endogen, Pierce, BioSource International, Zymed Laboratories, Caltag, Molecular Probes, Research Genetics, Life Technologies, Applied Biosystems, GIBCO BRL, ABgene, Dynal, Affinity BioReagents, Nunc, Invitrogen, NatuTec, Oxoid, Richard-Allan Scientific, Arcturus, Perseptive Biosystems, Proxeon, eBioscience

product type :

antibody

product name :

beta Amyloid Polyclonal Antibody (CT695)

catalog :

51-2700

quantity :

50 µg

price :

US 375.00

clonality :

polyclonal

host :

domestic rabbit

conjugate :

nonconjugated

clone name :

CT695

reactivity :

longfin inshore squid, human, mouse, rat, pigs

application :

western blot, ELISA, immunohistochemistry, immunocytochemistry, immunohistochemistry - frozen section, immunohistochemistry - free floating section

more info or order :

Invitrogen product webpage

citations: 35

Published Application/Species/Sample/Dilution	Reference
immunohistochemistry - frozen section; pigs ; 1:250; loading ...; fig 1a	Kallakuri S, Desai A, Feng K, Tummala S, Saif T, Chen C, et al. Neuronal Injury and Glial Changes Are Hallmarks of Open Field Blast Exposure in Swine Frontal Lobe. PLoS ONE. 2017;12:e0169239 pubmed publisher
immunohistochemistry - free floating section; mouse; loading ...; fig 2e	Hübner N, Mechling A, Lee H, Reisert M, Bienert T, Hennig J, et al. The connectomics of brain demyelination: Functional and structural patterns in the cuprizone mouse model. Neuroimage. 2017;146:1-18 pubmed publisher
western blot; human; loading ...; fig 3b	Tapia Rojas C, Burgos P, Inestrosa N. Inhibition of Wnt signaling induces amyloidogenic processing of amyloid precursor protein and the production and aggregation of Amyloid-? (A?)42 peptides. J Neurochem. 2016;139:1175-1191 pubmed publisher
western blot; mouse; loading ...; fig 3a	Qin X, Wang Y, Paudel H. Early Growth Response 1 (Egr-1) Is a Transcriptional Activator of ?-Secretase 1 (BACE-1) in the Brain. J Biol Chem. 2016;291:22276-22287 pubmed
immunocytochemistry; longfin inshore squid; fig 1	Stevenson J, Conaty E, Walsh R, Poidomani P, Samoriski C, Scollins B, et al. The Amyloid Precursor Protein of Alzheimer's Disease Clusters at the Organelle/Microtubule Interface on Organelles that Bind Microtubules in an ATP Dependent Manner. PLoS ONE. 2016;11:e0147808 pubmed publisher
	Bradshaw D, Knutsen A, Korotcov A, Sullivan G, Radomski K, Dardzinski B, et al. Genetic inactivation of SARM1 axon degeneration pathway improves outcome trajectory after experimental traumatic brain injury based on pathological, radiological, and functional measures. Acta Neuropathol Commun. 2021;9:89 pubmed publisher
	Cai C, Yang C, Zhuang X, Yuan N, Wu M, Tan J, et al. NRBF2 is a RAB7 effector required for autophagosome maturation and mediates the association of APP-CTFs with active form of RAB7 for degradation. Autophagy. 2020;:1-19 pubmed publisher
	Losurdo M, Davidsson J, Sköld M. Diffuse Axonal Injury in the Rat Brain: Axonal Injury and Oligodendrocyte Activity Following Rotational Injury. Brain Sci. 2020;10: pubmed publisher
	Song J, Malampati S, Zeng Y, Durairajan S, Yang C, Tong B, et al. A small molecule transcription factor EB activator ameliorates beta-amyloid precursor protein and Tau pathology in Alzheimer's disease models. Aging Cell. 2019;:e13069 pubmed publisher
	d Uscio L, Katusic Z. Vascular phenotype of amyloid precursor protein-deficient mice. Am J Physiol Heart Circ Physiol. 2019;316:H1297-H1308 pubmed publisher
	Anthony Jalin A, Jin R, Wang M, Li G. EPPS treatment attenuates traumatic brain injury in mice by reducing Aβ burden and ameliorating neuronal autophagic flux. Exp Neurol. 2019;314:20-33 pubmed publisher
	Chierto E, Simon A, Castoldi F, Meffre D, Cristinziano G, Sapone F, et al. Mechanical Stretch of High Magnitude Provokes Axonal Injury, Elongation of Paranodal Junctions, and Signaling Alterations in Oligodendrocytes. Mol Neurobiol. 2019;56:4231-4248 pubmed publisher
	Gorse K, Lafrenaye A. The Importance of Inter-Species Variation in Traumatic Brain Injury-Induced Alterations of Microglial-Axonal Interactions. Front Neurol. 2018;9:778 pubmed publisher
	McDonald W, Jones E, Wojciak J, Drake R, Sabbadini R, Harris N. Matrix-Assisted Laser Desorption Ionization Mapping of Lysophosphatidic Acid Changes after Traumatic Brain Injury and the Relationship to Cellular Pathology. Am J Pathol. 2018;188:1779-1793 pubmed publisher
	Kawa L, Kamnaksh A, Long J, Arborelius U, Hokfelt T, Agoston D, et al. A Comparative Study of Two Blast-Induced Traumatic Brain Injury Models: Changes in Monoamine and Galanin Systems Following Single and Repeated Exposure. Front Neurol. 2018;9:479 pubmed publisher
	Lyons D, Vekaria H, Macheda T, Bakshi V, Powell D, Gold B, et al. A mild traumatic brain injury in mice produces lasting deficits in brain metabolism. J Neurotrauma. 2018;: pubmed publisher
	Sauerbeck A, Fanizzi C, Kim J, Gangolli M, Bayly P, Wellington C, et al. modCHIMERA: a novel murine closed-head model of moderate traumatic brain injury. Sci Rep. 2018;8:7677 pubmed publisher
	Ziogas N, Koliatsos V. Primary Traumatic Axonopathy in Mice Subjected to Impact Acceleration: A Reappraisal of Pathology and Mechanisms with High-Resolution Anatomical Methods. J Neurosci. 2018;38:4031-4047 pubmed publisher
	Young J, Fong L, Frankowski H, Petsko G, Small S, Goldstein L. Stabilizing the Retromer Complex in a Human Stem Cell Model of Alzheimer's Disease Reduces TAU Phosphorylation Independently of Amyloid Precursor Protein. Stem Cell Reports. 2018;10:1046-1058 pubmed publisher
	Vascak M, Jin X, Jacobs K, Povlishock J. Mild Traumatic Brain Injury Induces Structural and Functional Disconnection of Local Neocortical Inhibitory Networks via Parvalbumin Interneuron Diffuse Axonal Injury. Cereb Cortex. 2018;28:1625-1644 pubmed publisher
	Tapia Rojas C, Inestrosa N. Wnt signaling loss accelerates the appearance of neuropathological hallmarks of Alzheimer's disease in J20-APP transgenic and wild-type mice. J Neurochem. 2017;: pubmed publisher
	Yang C, Cai C, Song J, Tan J, Durairajan S, Iyaswamy A, et al. NRBF2 is involved in the autophagic degradation process of APP-CTFs in Alzheimer disease models. Autophagy. 2017;13:2028-2040 pubmed publisher
	Haber M, Hutchinson E, Sadeghi N, Cheng W, Namjoshi D, Cripton P, et al. Defining an Analytic Framework to Evaluate Quantitative MRI Markers of Traumatic Axonal Injury: Preliminary Results in a Mouse Closed Head Injury Model. Eneuro. 2017;4: pubmed publisher
	Kallakuri S, Purkait H, Dalavayi S, VandeVord P, Cavanaugh J. Blast overpressure induced axonal injury changes in rat brainstem and spinal cord. J Neurosci Rural Pract. 2015;6:481-7 pubmed publisher
	Gyoneva S, Kim D, Katsumoto A, Kokiko Cochran O, Lamb B, Ransohoff R. Ccr2 deletion dissociates cavity size and tau pathology after mild traumatic brain injury. J Neuroinflammation. 2015;12:228 pubmed publisher
	Quigley H, Pitha I, Welsbie D, Nguyen C, Steinhart M, Nguyen T, et al. Losartan Treatment Protects Retinal Ganglion Cells and Alters Scleral Remodeling in Experimental Glaucoma. PLoS ONE. 2015;10:e0141137 pubmed publisher
	Lafrenaye A, Todani M, Walker S, Povlishock J. Microglia processes associate with diffusely injured axons following mild traumatic brain injury in the micro pig. J Neuroinflammation. 2015;12:186 pubmed publisher
	Rolyan H, Tyurina Y, Hernandez M, Amoscato A, Sparvero L, Nmezi B, et al. Defects of Lipid Synthesis Are Linked to the Age-Dependent Demyelination Caused by Lamin B1 Overexpression. J Neurosci. 2015;35:12002-17 pubmed publisher
	Cavieres V, GonzÃ¡lez A, MuÃ±oz V, Yefi C, Bustamante H, Barraza R, et al. Tetrahydrohyperforin Inhibits the Proteolytic Processing of Amyloid Precursor Protein and Enhances Its Degradation by Atg5-Dependent Autophagy. PLoS ONE. 2015;10:e0136313 pubmed publisher
	Del Mar N, von Buttlar X, Yu A, Guley N, Reiner A, Honig M. A novel closed-body model of spinal cord injury caused by high-pressure air blasts produces extensive axonal injury and motor impairments. Exp Neurol. 2015;271:53-71 pubmed publisher
	Bennett R, Brody D. Array tomography for the detection of non-dilated, injured axons in traumatic brain injury. J Neurosci Methods. 2015;245:25-36 pubmed publisher
	Cantoni C, Bollman B, Licastro D, Xie M, Mikesell R, Schmidt R, et al. TREM2 regulates microglial cell activation in response to demyelination in vivo. Acta Neuropathol. 2015;129:429-47 pubmed publisher
	HÃ¥nell A, Greer J, McGinn M, Povlishock J. Traumatic brain injury-induced axonal phenotypes react differently to treatment. Acta Neuropathol. 2015;129:317-32 pubmed publisher
	Kawa L, Arborelius U, Yoshitake T, Kehr J, HÃ¶kfelt T, Risling M, et al. Neurotransmitter Systems in a Mild Blast Traumatic Brain Injury Model: Catecholamines and Serotonin. J Neurotrauma. 2015;32:1190-9 pubmed publisher
	Yan Y, Eipper B, Mains R. Kalirin-9 and Kalirin-12 Play Essential Roles in Dendritic Outgrowth and Branching. Cereb Cortex. 2015;25:3487-501 pubmed publisher

product information

Product Type :

Antibody

Product Name :

beta Amyloid Polyclonal Antibody (CT695)

Catalog # :

51-2700

Quantity :

50 µg

Price :

US 375.00

Clonality :

Polyclonal

Purity :

Antigen affinity chromatography

Host :

Rabbit

Reactivity :

Human, Mouse, Porcine, Rat

Applications :

ELISA: 0.1-1.0 µg/mL, Immunohistochemistry: 0.1-1.0 µg/mL, Western Blot: 0.2-2 µg/mL

Species :

Human, Mouse, Porcine, Rat

Clone :

CT695

Isotype :

IgG

Storage :

-20°C

Description :

Amyloid beta peptide (Abeta/Beta-amyloid) is the major constituent of amyloid plaques in the brains of individuals afflicted with Alzheimer's disease. Abeta peptide is 40-43 amino acids long and generated from the beta-amyloid precursor protein (beta APP) in a two-step process. The first step involves cleavage of the extracellular, amino-terminal domain of beta APP. Protein cleavage is performed by an aspartyl protease, beta-secretase (BACE) which is synthesized as a propeptide and must be modified to the mature and active form by the prohormone convertase, furin. Beta APP cleavage by the mature form of BACE results in the cellular secretion of a segment of beta APP, and a membrane-bound remnant. The remnant protein is processed by another protease, gamma-secretase. Gamma-secretase cleaves an intra-membrane site in the carboxyl-terminal domain of beta APP, thus generating the amyloid beta peptide. Gamma-secretase is believed to be a multi-subunit complex containing presenilin-1 and 2 as central components. The transmembrane glycoprotein, nicastrin, is associated with presinilins and has been found to bind to the carboxyl-terminus of beta APP and helps to modulate the production of the amyloid beta peptide. Abeta is an extracellular filamentous protein component of amyloid cores, neuritic plaques and is also found as a deposit in neurofibrillary tangles. Alzheimer’s disease, the most common cause of senile dementia, is characterized by abnormal filamentous protein deposits in the brain. Beta amyloid deposits are also detected in Lewy body dementia, Down’s syndrome, amyloidosis (Dutch type), cerebroarterial amyloidosis (cerebral amyloid angiopathy) and in the Guam Parkinson-Dementia complex.

Immunogen :

A 22 amino acid synthetic peptide derived from the C-terminus of the human beta-amyloid precursor protein (beta-APP). This sequence is 100% conserved in human, monkey, mouse, rat, guinea pig, and chicken beta-APP proteins.

Format :

Liquid

Applications w/Dilutions :

ELISA: 0.1-1.0 µg/mL, Immunohistochemistry: 0.1-1.0 µg/mL, Western Blot: 0.2-2 µg/mL

Aliases :

A4; AAA; ABETA; Abeta40; Abeta42; ABPP; AD1; Adap; AG; AICD-50; AICD-57; AICD-59; AID(50); AID(57); AID(59); Alpha-CTF; Alpha-secretase C-terminal fragment; Alzheimer disease; Alzheimer disease amyloid A4 protein homolog; alzheimer disease amyloid protein; Amyloid; amyloid A4; Amyloid b; Amyloid beta; amyloid beta (A4) precursor protein; amyloid beta (A4) precursor protein (peptidase nexin-II, Alzheimer disease); amyloid beta A4 protein; amyloid beta precursor protein; Amyloid intracellular domain 50; Amyloid intracellular domain 57; Amyloid intracellular domain 59; Amyloid precursor protein; amyloid precursor protein variant 1; amyloid precursor protein variant 2; Amyloid ß; amyloid-beta A4 protein; amyloid-beta A4 protein; amyloid beta A4 protein; Amyloid-beta precursor protein; Amyloid-beta protein 40; Amyloid-beta protein 42; Amyloidogenic glycoprotein; APP; APP-C57; APP-C59; APP-C99; APPI; appican; beta amyloid protein; beta amyloid protein precursor; beta-amyloid peptide; beta-amyloid peptide(1-40); beta-amyloid peptide(1-42); Beta-amyloid precursor protein; betaApp; Beta-APP40; Beta-APP42; Beta-CTF; Beta-secretase C-terminal fragment; C31; C80; C83; C99; Cerebral vascular amyloid peptide; CTF gamma; CTF-alpha; CTFgamma; CVAP; E030013M08Rik; Gamma-CTF(50); Gamma-CTF(57); Gamma-CTF(59); Gamma-secretase C-terminal fragment 50; Gamma-secretase C-terminal fragment 57; Gamma-secretase C-terminal fragment 59; N-APP; OTTHUMP00000096096; P3(40); P3(42); Pan-Abeta; peptidase nexin-II; PN2; PN-II; PreA4; PreA4 751; protease nexin II; protease nexin-II; S-APP-alpha; S-APP-beta; Soluble APP-alpha; Soluble APP-beta; testicular tissue protein Li 2

more info or order :

Invitrogen product webpage