Chk X Presenilin 1

Species Reactivity	Key Applications	Host	Format	Antibody Type
H, M, R	ELISA, WB	Ch	Affinity Purified	Polyclonal Antibody

Species Reactivity

Key Applications

Host

Format

Antibody Type

H, M, R

ELISA, WB

Affinity Purified

Polyclonal Antibody

Description
Catalogue Number	AB5757
Brand Family	Chemicon®
Trade Name	Chemicon
Description	Anti-Presenilin 1 Antibody

Description

Catalogue Number

AB5757

Brand Family

Chemicon®

Trade Name

Chemicon

Description

Anti-Presenilin 1 Antibody

Product Information
Format	Affinity Purified
Presentation	Affinity purified immunoglobulin. Liquid in PBS containing 0.02% sodium azide.

Product Information

Format

Affinity Purified

Presentation

Affinity purified immunoglobulin. Liquid in PBS containing 0.02% sodium azide.

Applications
Application	Detect Presenilin 1 using this Anti-Presenilin 1 Antibody validated for use in ELISA & WB.
Key Applications	ELISA Western Blotting
Application Notes	Immunoblotting: 1:1,000-1:4,000. To minimize background staining it is suggested that you include a higher content of detergent (Tween-20) in your dilution and washing solutions. Immunohistochemistry: not tested. It is recommended that you try the antibody at 1:50-1:500. ELISA: 1:1,000-1:4,000 Optimal working dilutions must be determined by the end user.

Applications

Application

Detect Presenilin 1 using this Anti-Presenilin 1 Antibody validated for use in ELISA & WB.

Key Applications

ELISA
Western Blotting

Application Notes

Immunoblotting: 1:1,000-1:4,000. To minimize background staining it is suggested that you include a higher content of detergent (Tween-20) in your dilution and washing solutions.

Immunohistochemistry: not tested. It is recommended that you try the antibody at 1:50-1:500.

ELISA: 1:1,000-1:4,000

Optimal working dilutions must be determined by the end user.

Biological Information
Immunogen	Synthetic peptides from human Presenilin 1.
Concentration	Please refer to the Certificate of Analysis for the lot-specific concentration.
Host	Chicken
Specificity	Presenilin 1
Species Reactivity	Human Mouse Rat
Antibody Type	Polyclonal Antibody
Entrez Gene Number	NM_000021.2
Entrez Gene Summary	Alzheimer's disease (AD) patients with an inherited form of the disease carry mutations in the presenilin proteins (PSEN1; PSEN2) or in the amyloid precursor protein (APP). These disease-linked mutations result in increased production of the longer form of amyloid-beta (main component of amyloid deposits found in AD brains). Presenilins are postulated to regulate APP processing through their effects on gamma-secretase, an enzyme that cleaves APP. Also, it is thought that the presenilins are involved in the cleavage of the Notch receptor, such that they either directly regulate gamma-secretase activity or themselves are protease enzymes. Multiple alternatively spliced transcript variants have been identified for this gene, the full-length natures of only some have been determined.
Gene Symbol	PSEN1 PS1 PSNL1 PS-1 AD3 FAD S182 Presenilin-1 EC 3.4.23.- [Contains: Presenilin-1 NTF subunit Presenilin-1 CTF subunit Presenilin-1 CTF12 (PS1-CTF12)].
UniProt Number	P49768
UniProt Summary	FUNCTION: SwissProt: P49768 # Probable catalytic subunit of the gamma-secretase complex, an endoprotease complex that catalyzes the intramembrane cleavage of integral membrane proteins such as Notch receptors and APP (beta-amyloid precursor protein). Requires the other members of the gamma-secretase complex to have a protease activity. May play a role in intracellular signaling and gene expression or in linking chromatin to the nuclear membrane. Stimulates cell-cell adhesion though its association with the E-cadherin/catenin complex. Under conditions of apoptosis or calcium influx, cleaves E-cadherin promoting the disassembly of the E-cadherin/catenin complex and increasing the pool of cytoplasmic beta-catenin, thus negatively regulating Wnt signaling. May also play a role in hematopoiesis. SIZE: 467 amino acids; 52668 Da SUBUNIT: Homodimer. Component of the gamma-secretase complex, a complex composed of a presenilin homodimer (PSEN1 or PSEN2), nicastrin (NCSTN), APH1 (APH1A or APH1B) and PEN2. Such minimal complex is sufficient for secretase activity. Other components which are associated with the complex include SLC25A64, SLC5A7, PHB and PSEN1 isoform 3. Predominantly heterodimer of a N-terminal (NTF) and a C-terminal (CTF) endoproteolytical fragment. Associates with proteolytic processed C-terminal fragments C83 and C99 of the amyloid precursor protein (APP). Associates with NOTCH1. Component of cadherin/catenin adhesion complexes through direct binding to CDH1 or CDH2. Interaction with CDH1 stabilizes the complex and stimulates cell-cell aggregation. Interaction with CDH2 is essential for trafficking of CDH2 from the endoplasmic reticulum to the plasma membrane. Interacts with CTNND2, CTNNB1, HERPUD1, FLNA, FLNB, MTCH1, PKP4 and PARL. Interacts through its N-terminus with isoform 3 of GFAP. Interacts with DOCK3 (By similarity). SUBCELLULAR LOCATION: Endoplasmic reticulum membrane; Multi-pass membrane protein. Golgi apparatus membrane; Multi-pass membrane protein. Cell surface. Note=Bound to NOTCH1 also at the cell surface. Colocalizes with CDH1/2 at sites of cell-cell contact. Colocalizes with CTNNB1 in the endoplasmic reticulum and the proximity of the plasma membrane. Also present in azurophil granules of neutrophils. TISSUE SPECIFICITY: Expressed in a wide range of tissues including various regions of the brain, liver, spleen and lymph nodes. DOMAIN: SwissProt: P49768 The PAL motif is required for normal active site conformation. PTM: Heterogeneous proteolytic processing generates N-terminal (NTF) and C-terminal (CTF) fragments of approximately 35 and 20 kDa, respectively. During apoptosis, the C-terminal fragment (CTF) is further cleaved by caspase-3 to produce the fragment, PS1- CTF12. & After endoproteolysis, the C-terminal fragment (CTF) is phosphorylated on serine residues by PKA and/or PKC. Phosphorylation on Ser-346 inhibits endoproteolysis. DISEASE: SwissProt: P49768 # Defects in PSEN1 are a cause of familial early-onset Alzheimer disease type 3 (AD3) [MIM:607822]. AD3 is the most severe form of the disease, with complete penetrance and an onset occurring as early as 30 years of age. The second form is late- onset AD (LOAD), with mean age of onset greater than 58 years. AD is an autosomal dominant neurodegenerative disorder characterized by progressive dementia, parkinsonism, and deposition of fibrillar amyloid proteins as intraneuronal neurofibrillary tangles, extracellular amyloid plaques and vascular amyloid deposits. The major protein found within these deposits is a small, insoluble and highly aggregating polypeptide, beta-amyloid protein (beta- APP42). Defects in PSEN1 result in an overproduction of beta- APP42. Variant Pro-166, a very aggressive mutation that causes onset of AD3 in adolescence, not only induces an exceptionally high increase of beta-APP42 production, but also impairs Notch intracellular domain production and Notch signaling, as well as beta-APP intracellular domain generation. & Defects in PSEN1 are a cause of frontotemporal dementia [MIM:600274]. SIMILARITY: Belongs to the peptidase A22A family.

Biological Information

Immunogen

Synthetic peptides from human Presenilin 1.

Concentration

Please refer to the Certificate of Analysis for the lot-specific concentration.

Host

Chicken

Specificity

Presenilin 1

Species Reactivity

Human
Mouse
Rat

Antibody Type

Polyclonal Antibody

Entrez Gene Number

NM_000021.2

Entrez Gene Summary

Alzheimer's disease (AD) patients with an inherited form of the disease carry mutations in the presenilin proteins (PSEN1; PSEN2) or in the amyloid precursor protein (APP). These disease-linked mutations result in increased production of the longer form of amyloid-beta (main component of amyloid deposits found in AD brains). Presenilins are postulated to regulate APP processing through their effects on gamma-secretase, an enzyme that cleaves APP. Also, it is thought that the presenilins are involved in the cleavage of the Notch receptor, such that they either directly regulate gamma-secretase activity or themselves are protease enzymes. Multiple alternatively spliced transcript variants have been identified for this gene, the full-length natures of only some have been determined.

Gene Symbol

PSEN1
PS1
PSNL1
PS-1
AD3
FAD
S182
Presenilin-1
EC 3.4.23.- [Contains: Presenilin-1 NTF subunit
Presenilin-1 CTF subunit
Presenilin-1 CTF12 (PS1-CTF12)].

UniProt Number

P49768

UniProt Summary

FUNCTION: SwissProt: P49768 # Probable catalytic subunit of the gamma-secretase complex, an endoprotease complex that catalyzes the intramembrane cleavage of integral membrane proteins such as Notch receptors and APP (beta-amyloid precursor protein). Requires the other members of the gamma-secretase complex to have a protease activity. May play a role in intracellular signaling and gene expression or in linking chromatin to the nuclear membrane. Stimulates cell-cell adhesion though its association with the E-cadherin/catenin complex. Under conditions of apoptosis or calcium influx, cleaves E-cadherin promoting the disassembly of the E-cadherin/catenin complex and increasing the pool of cytoplasmic beta-catenin, thus negatively regulating Wnt signaling. May also play a role in hematopoiesis.
SIZE: 467 amino acids; 52668 Da
SUBUNIT: Homodimer. Component of the gamma-secretase complex, a complex composed of a presenilin homodimer (PSEN1 or PSEN2), nicastrin (NCSTN), APH1 (APH1A or APH1B) and PEN2. Such minimal complex is sufficient for secretase activity. Other components which are associated with the complex include SLC25A64, SLC5A7, PHB and PSEN1 isoform 3. Predominantly heterodimer of a N-terminal (NTF) and a C-terminal (CTF) endoproteolytical fragment. Associates with proteolytic processed C-terminal fragments C83 and C99 of the amyloid precursor protein (APP). Associates with NOTCH1. Component of cadherin/catenin adhesion complexes through direct binding to CDH1 or CDH2. Interaction with CDH1 stabilizes the complex and stimulates cell-cell aggregation. Interaction with CDH2 is essential for trafficking of CDH2 from the endoplasmic reticulum to the plasma membrane. Interacts with CTNND2, CTNNB1, HERPUD1, FLNA, FLNB, MTCH1, PKP4 and PARL. Interacts through its N-terminus with isoform 3 of GFAP. Interacts with DOCK3 (By similarity).
SUBCELLULAR LOCATION: Endoplasmic reticulum membrane; Multi-pass membrane protein. Golgi apparatus membrane; Multi-pass membrane protein. Cell surface. Note=Bound to NOTCH1 also at the cell surface. Colocalizes with CDH1/2 at sites of cell-cell contact. Colocalizes with CTNNB1 in the endoplasmic reticulum and the proximity of the plasma membrane. Also present in azurophil granules of neutrophils.
TISSUE SPECIFICITY: Expressed in a wide range of tissues including various regions of the brain, liver, spleen and lymph nodes.
DOMAIN: SwissProt: P49768 The PAL motif is required for normal active site conformation.
PTM: Heterogeneous proteolytic processing generates N-terminal (NTF) and C-terminal (CTF) fragments of approximately 35 and 20 kDa, respectively. During apoptosis, the C-terminal fragment (CTF) is further cleaved by caspase-3 to produce the fragment, PS1- CTF12. & After endoproteolysis, the C-terminal fragment (CTF) is phosphorylated on serine residues by PKA and/or PKC. Phosphorylation on Ser-346 inhibits endoproteolysis.
DISEASE: SwissProt: P49768 # Defects in PSEN1 are a cause of familial early-onset Alzheimer disease type 3 (AD3) [MIM:607822]. AD3 is the most severe form of the disease, with complete penetrance and an onset occurring as early as 30 years of age. The second form is late- onset AD (LOAD), with mean age of onset greater than 58 years. AD is an autosomal dominant neurodegenerative disorder characterized by progressive dementia, parkinsonism, and deposition of fibrillar amyloid proteins as intraneuronal neurofibrillary tangles, extracellular amyloid plaques and vascular amyloid deposits. The major protein found within these deposits is a small, insoluble and highly aggregating polypeptide, beta-amyloid protein (beta- APP42). Defects in PSEN1 result in an overproduction of beta- APP42. Variant Pro-166, a very aggressive mutation that causes onset of AD3 in adolescence, not only induces an exceptionally high increase of beta-APP42 production, but also impairs Notch intracellular domain production and Notch signaling, as well as beta-APP intracellular domain generation. & Defects in PSEN1 are a cause of frontotemporal dementia [MIM:600274].
SIMILARITY: Belongs to the peptidase A22A family.

Product Usage Statements
Usage Statement	Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

Product Usage Statements

Usage Statement

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

Storage and Shipping Information
Storage Conditions	Maintain at -20°C in undiluted aliquots for up to 6 months after date of receipt. Avoid repeated freeze/thaw cycles.

Storage and Shipping Information

Storage Conditions

Maintain at -20°C in undiluted aliquots for up to 6 months after date of receipt. Avoid repeated freeze/thaw cycles.

Packaging Information
Material Size	100 µg

Packaging Information

Material Size

100 µg

实验耗材

分子生物学试剂

蛋白与免疫学

生化试剂

细胞及检测试剂

色谱及层析

仪器设备

实验服务

办公用品

浏览了该商品的用户最终购买

浏览了该商品的用户还浏览了

特卖

重要规格表

我要咨询