Phospho-Synuclein alpha (Ser129) Antibody - #AF3285

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Product: Phospho-Synuclein alpha (Ser129) Antibody
Catalog: AF3285
Description: Rabbit polyclonal antibody to Phospho-Synuclein alpha (Ser129)
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Horse, Rabbit, Dog, Chicken
Mol.Wt.: 18kDa; 14kD(Calculated).
Uniprot: P37840
RRID: AB_2834706

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 100ul $280 In stock
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Related Downloads
MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Prediction:
Pig(100%), Bovine(100%), Horse(100%), Rabbit(100%), Dog(100%), Chicken(85%)
Clonality:
Polyclonal
Specificity:
Phospho-Synuclein alpha (Ser129) Antibody detects endogenous levels of Synuclein alpha only when phosphorylated at Serine 129.
RRID:
AB_2834706
Cite Format: Affinity Biosciences Cat# AF3285, RRID:AB_2834706.
Conjugate:
Unconjugated.
Purification:
The antibody is from purified rabbit serum by affinity purification via sequential chromatography on phospho-peptide and non-phospho-peptide affinity columns.
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

Alpha synuclein; Alpha-synuclein; Alpha-synuclein, isoform NACP140; alphaSYN; MGC105443; MGC110988; MGC127560; MGC64356; NACP; Non A beta component of AD amyloid; Non A4 component of amyloid; Non A4 component of amyloid precursor; Non-A beta component of AD amyloid; Non-A-beta component of alzheimers disease amyloid , precursor of; Non-A4 component of amyloid precursor; Non-A4 component of amyloid, precursor of; OTTHUMP00000218549; OTTHUMP00000218551; OTTHUMP00000218552; OTTHUMP00000218553; OTTHUMP00000218554; PARK 1; PARK 4; PARK1; PARK4; Parkinson disease (autosomal dominant, Lewy body) 4; Parkinson disease familial 1; SNCA; Snca synuclein, alpha (non A4 component of amyloid precursor); SYN; Synuclein alpha; Synuclein alpha 140; Synuclein, alpha (non A4 component of amyloid precursor); SYUA_HUMAN;

Immunogens

Immunogen:
Uniprot:

P37840(SYUA_HUMAN) >>Visit HPA database.

Gene(ID):
SNCA(6622)
Expression:
P37840 SYUA_HUMAN:

Highly expressed in presynaptic terminals in the central nervous system. Expressed principally in brain.

Description:
Alpha-synuclein is a member of the synuclein family, which also includes beta- and gamma-synuclein. Synucleins are abundantly expressed in the brain and alpha- and beta-synuclein inhibit phospholipase D2 selectively.
Sequence:
MDVFMKGLSKAKEGVVAAAEKTKQGVAEAAGKTKEGVLYVGSKTKEGVVHGVATVAEKTKEQVTNVGGAVVTGVTAVAQKTVEGAGSIAAATGFVKKDQLGKNEEGAPQEGILEDMPVDPDNEAYEMPSEEGYQDYEPEA

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Pig
100
Horse
100
Bovine
100
Dog
100
Rabbit
100
Chicken
85
Xenopus
77
Sheep
0
Zebrafish
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - P37840 As Substrate

Site PTM Type Enzyme
Ubiquitination
M1 Acetylation
K6 Sumoylation
K10 Sumoylation
K12 Sumoylation
K12 Ubiquitination
K21 Acetylation
K21 Sumoylation
K21 Ubiquitination
K23 Sumoylation
K23 Ubiquitination
K34 Sumoylation
Y39 Phosphorylation
S42 Phosphorylation
K45 Sumoylation
T54 O-Glycosylation
K58 Acetylation
K60 Sumoylation
K80 Sumoylation
S87 O-Glycosylation
S87 Phosphorylation P48729 (CSNK1A1) , P68400 (CSNK2A1) , Q13627 (DYRK1A)
K96 Acetylation
K96 Sumoylation
K102 Sumoylation
Y125 Phosphorylation P06241 (FYN) , Q14289 (PTK2B) , P12931 (SRC) , P43405 (SYK)
S129 Phosphorylation P68400 (CSNK2A1) , P49841 (GSK3B) , P53350 (PLK1) , Q5S007 (LRRK2) , P25098 (GRK2) , P34947 (GRK5) , P48729 (CSNK1A1) , Q9UQM7 (CAMK2A) , P43250 (GRK6) , Q9H4B4 (PLK3) , Q9NYY3 (PLK2)
Y133 Phosphorylation P43405 (SYK)
Y136 Phosphorylation P43405 (SYK)

Research Backgrounds

Function:

Neuronal protein that plays several roles in synaptic activity such as regulation of synaptic vesicle trafficking and subsequent neurotransmitter release. Participates as a monomer in synaptic vesicle exocytosis by enhancing vesicle priming, fusion and dilation of exocytotic fusion pores. Mechanistically, acts by increasing local Ca(2+) release from microdomains which is essential for the enhancement of ATP-induced exocytosis. Acts also as a molecular chaperone in its multimeric membrane-bound state, assisting in the folding of synaptic fusion components called SNAREs (Soluble NSF Attachment Protein REceptors) at presynaptic plasma membrane in conjunction with cysteine string protein-alpha/DNAJC5. This chaperone activity is important to sustain normal SNARE-complex assembly during aging. Plays also a role in the regulation of the dopamine neurotransmission by associating with the dopamine transporter (DAT1) and thereby modulating its activity.

PTMs:

Phosphorylated, predominantly on serine residues. Phosphorylation by CK1 appears to occur on residues distinct from the residue phosphorylated by other kinases. Phosphorylation of Ser-129 is selective and extensive in synucleinopathy lesions. In vitro, phosphorylation at Ser-129 promoted insoluble fibril formation. Phosphorylated on Tyr-125 by a PTK2B-dependent pathway upon osmotic stress.

Hallmark lesions of neurodegenerative synucleinopathies contain alpha-synuclein that is modified by nitration of tyrosine residues and possibly by dityrosine cross-linking to generated stable oligomers.

Ubiquitinated. The predominant conjugate is the diubiquitinated form (By similarity).

Acetylation at Met-1 seems to be important for proper folding and native oligomeric structure.

Subcellular Location:

Cytoplasm. Membrane. Nucleus. Cell junction>Synapse. Secreted.
Note: Membrane-bound in dopaminergic neurons.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Highly expressed in presynaptic terminals in the central nervous system. Expressed principally in brain.

Subunit Structure:

Soluble monomer. Homotetramer. A dynamic intracellular population of tetramers and monomers coexists normally and the tetramer plays an essential role in maintaining homeostasis. Interacts with UCHL1 (By similarity). Interacts with phospholipase D and histones. Interacts (via N-terminus) with synphilin-1/SNCAIP; this interaction promotes formation of SNCA inclusions in the cytoplasm. Interacts with CALM1. Interacts with STXBP1; this interaction controls SNCA self-replicating aggregation. Interacts with SNARE components VAMP2 and SNAP25; these interactions allows SNARE complex assembly and integrity. Interacts with RPH3A and RAB3A. Interacts with SERF1A; this interaction promotes the aggregation of SNCA.

Family&Domains:

The 'non A-beta component of Alzheimer disease amyloid plaque' domain (NAC domain) is involved in fibrils formation. The middle hydrophobic region forms the core of the filaments. The C-terminus may regulate aggregation and determine the diameter of the filaments.

Belongs to the synuclein family.

Research Fields

· Human Diseases > Neurodegenerative diseases > Alzheimer's disease.

· Human Diseases > Neurodegenerative diseases > Parkinson's disease.

References

1). An artificial protein modulator reprogramming neuronal protein functions. Nature communications, 2024 (PubMed: 38448420) [IF=16.6]

Application: WB    Species: Mouse    Sample:

Fig. 5 APROM2 reprograms neuronal protein functions via de novo PTMs to fuel synaptic function. a Schematic illustration of the de novo PTM strategy of neuronal proteins using APROM2. APROM2 with protein phosphatase-like characteristics can dephosphorylate phospho-proteins, and thus restore the function of neuronal proteins. Created with BioRender.com. b Top, representative confocal laser scanning microscopy (CLSM) images of p-α-syn in primary neurons after different treatments. Bottom, 3D mapping of intracellular fluorescence. c Mean fluorescence intensity of p-α-syn in primary neurons after different treatments (n = 5 biologically independent cultures). Quantitative analysis (d) and representative CLSM images (e) of synaptic vesicle function indicated by FM1-43 after different treatments (n = 5 biologically independent cultures). Immunofluorescence and quantification analysis of the colocalization of α-syn with VMAT2 (f, h) or VAMP2 (g, i) in primary neurons after different treatments (n = 5 biologically independent cultures). j Microscopy images showing the neurite branches and neuronal connectivity of primary neurons after different treatments. k Intracellular ROS levels in primary neurons after different treatments. l, m Mitochondrial membrane potential (∆ψ) is indicated by JC-1 staining (l) and quantified by normalized JC-1 aggregates/monomers ratio (m) (n = 3 biologically independent cultures). JC-1 monomers (green) represent low ∆ψ, and JC-1 aggregates (red) represent high ∆ψ. n Protective effect of APROM2 and CeNPs on MPP+ treated cells (n = 5 biologically independent cultures). o Schematic illustration of APROM2 that reprograms α-syn function by the de novo PTM strategy and protects mitochondria for fueling synaptic function. APROM2 directly modulates p-α-syn by cleaving the phosphate monoester bond, thus, α-syn regains biological functions of binding to VMAT2 and VAMP2. In addition, APROM2 protects mitochondria against ROS to maintain presynaptic energy homeostasis. All the data are presented as means ± s.e.m. Statistical significance was analyzed by one-way ANOVA with multiple comparisons test. Source data are provided as a Source Data file.
2). Intranasal Administration of GRP78 Protein (HSPA5) Confers Neuroprotection in a Lactacystin-Induced Rat Model of Parkinson's Disease. International journal of molecular sciences, 2024 (PubMed: 38612761) [IF=5.6]

Application: WB    Species: Rat    Sample: nigral tissue

Figure 3 Exogenous GRP78 prevents abnormal accumulation of α-syn phosphorylated at S129 (pS129) in nigral tissue in rat model of Parkinson’s disease. Nigral content of (a) soluble form of α-syn, (b) α-syn phosphorylated at S129 (pS129), (c) phosphorylated to soluble α-syn ratio. Western blot analysis of nigral tissue was conducted with the antibodies against soluble and S129-phosphorylated forms of α-syn. Anti-GAPDH antibody staining was used as the loading control. (d) Representative Western blots are shown in panel. The results are presented as percentages of the control (100%) in (a–c) panels. Bar charts indicate mean values with standard errors. The dots, squares, triangles and rhombus show individual values per rat. Two-way ANOVA test followed by Tukey’s post hoc analysis were performed to determine the effects of GRP78 therapy. Asterisks indicate significant differences between groups according to Tukey’s post hoc tests

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