Presenilin 2 Antibody [M18A3] | Primary Antibodies

Application: Reactivity: Mouse, Rat, Human

Usage Information

Dilution
WB1:20000 IP1:20 IHC1:500 IF1:50 - 1:250 FCM1:50

Application
WB, IP, IHC, IF, FCM

Reactivity
Mouse, Rat, Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
50 kDa 23 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight.

Positive Control	Human Alzheimer's brain tissue; Human cerebrum tissue; HeLa cells; HepG2 cells; C2C12 cells; C6 cells; Neuro-2a cells; U-87 MG cells; A549 cells; PC-12 cells
Negative Control	MOLT-4 cells

Datasheet & SDS

Biological Description

Specificity
Presenilin 2 Antibody [M18A3] detects endogenous levels of total Presenilin 2 protein.

Clone
M18A3

Synonym(s)
AD4; PS2; PSNL2; STM2; PSEN2; Presenilin-2; PS-2; AD3LP; AD5; E5-1; STM-2

Background
Presenilin 2 (PSEN2), together with presenilin 1 (PSEN1), belongs to the presenilin family of multipass transmembrane aspartyl proteases acting as the catalytic subunit of the γ-secretase complex, which also includes nicastrin, APH-1, and PEN-2, to execute intramembrane proteolysis of type-I transmembrane proteins like APP and NOTCH. PSEN2 features nine transmembrane domains undergoing endoproteolysis into N-terminal (~34 kDa) and C-terminal (~20-23 kDa) fragments that heterodimerize in the active complex, with catalytic aspartates at Asp257 (TM6) and Asp385 (TM7), distinct transmembrane helix tilts from PS1, and intracellular charge anchoring directing localization to trans-Golgi/recycling endosomes. Its core functions emphasize γ-secretase-mediated cleavage of APP-C99 to produce Aβ40/42 peptides regulating synaptic plasticity (physiological) yet driving plaque formation when dysregulated, alongside intramembrane cleaving of NOTCH to liberate NICD for transcriptional activation of cell fate, neurogenesis, and differentiation genes. PSEN2 integrates amyloidogenic and NOTCH pathways, modulates vascular signaling, and represses inflammation via microglial feedback. Disease relevance centers on familial Alzheimer's disease (FAD) mutations shifting Aβ profiles toward neurotoxic Aβ42 accumulation, with PSEN2 predominance in microglia exacerbating neuroinflammation; unlike PS1's plasma membrane targeting, PS2 localizes intracellularly, influencing substrate specificity and cardiovascular pathologies.

Background

Presenilin 2 (PSEN2), together with presenilin 1 (PSEN1), belongs to the presenilin family of multipass transmembrane aspartyl proteases acting as the catalytic subunit of the γ-secretase complex, which also includes nicastrin, APH-1, and PEN-2, to execute intramembrane proteolysis of type-I transmembrane proteins like APP and NOTCH. PSEN2 features nine transmembrane domains undergoing endoproteolysis into N-terminal (~34 kDa) and C-terminal (~20-23 kDa) fragments that heterodimerize in the active complex, with catalytic aspartates at Asp257 (TM6) and Asp385 (TM7), distinct transmembrane helix tilts from PS1, and intracellular charge anchoring directing localization to trans-Golgi/recycling endosomes. Its core functions emphasize γ-secretase-mediated cleavage of APP-C99 to produce Aβ40/42 peptides regulating synaptic plasticity (physiological) yet driving plaque formation when dysregulated, alongside intramembrane cleaving of NOTCH to liberate NICD for transcriptional activation of cell fate, neurogenesis, and differentiation genes. PSEN2 integrates amyloidogenic and NOTCH pathways, modulates vascular signaling, and represses inflammation via microglial feedback. Disease relevance centers on familial Alzheimer's disease (FAD) mutations shifting Aβ profiles toward neurotoxic Aβ42 accumulation, with PSEN2 predominance in microglia exacerbating neuroinflammation; unlike PS1's plasma membrane targeting, PS2 localizes intracellularly, influencing substrate specificity and cardiovascular pathologies.

References
https://pubmed.ncbi.nlm.nih.gov/27059953/ https://pubmed.ncbi.nlm.nih.gov/35515530/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%