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- Antibody Data
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- References [6]
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- Immunohistochemistry [1]
- Other assay [9]
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- Product number
- MA1-90346 - Provider product page
- Provider
- Invitrogen Antibodies
- Product name
- alpha Synuclein Monoclonal Antibody (4B12)
- Antibody type
- Monoclonal
- Antigen
- Recombinant full-length protein
- Description
- Predicted molecular weight of 16 kDa.
- Reactivity
- Human
- Host
- Mouse
- Isotype
- IgG
- Antibody clone number
- 4B12
- Vial size
- 100 µL
- Concentration
- 1 mg/mL
- Storage
- Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles.
Submitted references Lipase regulation of cellular fatty acid homeostasis as a Parkinson's disease therapeutic strategy.
Establishment of a human induced pluripotent stem cell neuronal model for identification of modulators of A53T α-synuclein levels and aggregation.
Altered conformation of α-synuclein drives dysfunction of synaptic vesicles in a synaptosomal model of Parkinson's disease.
Clinicopathological Staging of Dynamics of Neurodegeneration and Neuronal Loss in Alzheimer Disease.
Nilotinib Fails to Prevent Synucleinopathy and Cell Loss in a Mouse Model of Multiple System Atrophy.
A prolyl oligopeptidase inhibitor, KYP-2047, reduces α-synuclein protein levels and aggregates in cellular and animal models of Parkinson's disease.
Fanning S, Cirka H, Thies JL, Jeong J, Niemi SM, Yoon J, Ho GPH, Pacheco JA, Dettmer U, Liu L, Clish CB, Hodgetts KJ, Hutchinson JN, Muratore CR, Caldwell GA, Caldwell KA, Selkoe D
NPJ Parkinson's disease 2022 Jun 9;8(1):74
NPJ Parkinson's disease 2022 Jun 9;8(1):74
Establishment of a human induced pluripotent stem cell neuronal model for identification of modulators of A53T α-synuclein levels and aggregation.
Vajhøj C, Schmid B, Alik A, Melki R, Fog K, Holst B, Stummann TC
PloS one 2021;16(12):e0261536
PloS one 2021;16(12):e0261536
Altered conformation of α-synuclein drives dysfunction of synaptic vesicles in a synaptosomal model of Parkinson's disease.
Fonseca-Ornelas L, Viennet T, Rovere M, Jiang H, Liu L, Nuber S, Ericsson M, Arthanari H, Selkoe DJ
Cell reports 2021 Jul 6;36(1):109333
Cell reports 2021 Jul 6;36(1):109333
Clinicopathological Staging of Dynamics of Neurodegeneration and Neuronal Loss in Alzheimer Disease.
Wegiel J, Flory M, Kuchna I, Nowicki K, Ma SY, Wegiel J, Badmaev E, Leon M, Wisniewski T, Reisberg B
Journal of neuropathology and experimental neurology 2021 Jan 1;80(1):21-44
Journal of neuropathology and experimental neurology 2021 Jan 1;80(1):21-44
Nilotinib Fails to Prevent Synucleinopathy and Cell Loss in a Mouse Model of Multiple System Atrophy.
Lopez-Cuina M, Guerin PA, Canron MH, Delamarre A, Dehay B, Bezard E, Meissner WG, Fernagut PO
Movement disorders : official journal of the Movement Disorder Society 2020 Jul;35(7):1163-1172
Movement disorders : official journal of the Movement Disorder Society 2020 Jul;35(7):1163-1172
A prolyl oligopeptidase inhibitor, KYP-2047, reduces α-synuclein protein levels and aggregates in cellular and animal models of Parkinson's disease.
Myöhänen TT, Hannula MJ, Van Elzen R, Gerard M, Van Der Veken P, García-Horsman JA, Baekelandt V, Männistö PT, Lambeir AM
British journal of pharmacology 2012 Jun;166(3):1097-113
British journal of pharmacology 2012 Jun;166(3):1097-113
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Supportive validation
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Immunohistochemistry analysis of the cortical Lewy body using alpha Synuclein Monoclonal Antibody (4B12) (Product # MA1-90346).
Supportive validation
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- NULL
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- NULL
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- NULL
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- NULL
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- NULL
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Figure 3. Exogenous alphaSyn is delivered into and remains inside synaptosomes (A) Semiquantitative western blot of intra-synaptosomal alphaSyn after electroporation and subsequent washes and trypsin treatment. Data are shown for 3 biological replicates. Note the short products of alphaSyn cleavage in the trypsin digestion lanes. (B) Time course of recombinant alphaSyn and endogenous glutaminase and SNAP25 retention after electroporation. Less than 15% of alphaSyn, glutaminase, and SNAP25 signal is lost from the synaptosomes during the first 4 h of incubation post-electroporation, the time interval employed in our NMR experiments. In the quantification plot, solid lines represent the signal in the pellet measured at the given times after electroporation, while the dashed lines depict signal intensities from the corresponding supernatants, reflecting protein leakage. (C) Immunofluorescent microscopy of alphaSyn inside synaptosomes from 12-month-old NTG mice. 4B12 (green channel) recognizes only the human (recombinant) alphaSyn, while C20 (red channel) recognizes both mouse and human alphaSyn. The panel to the far left shows synaptosomes in the presence of recombinant alphaSyn without electroporation and washing steps (i.e., alphaSyn accumulates on the synaptosomal outer membrane). The adjacent panel shows electroporated synaptosomes, where recombinant alphaSyn adopts the same uniform localization as endogenous murine alphaSyn (immunofluorescence shows complete colocalization,
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- 10.1371/journal.pone.0261536.g001 Fig 1 Establishment and differentiation into neurons of iPSC line BIONi010-C-24 with doxycycline inducible A53T alpha-synuclein. (A) Illustration of the doxycycline (DOX) inducible SNCA expression system: One allele contained the m2 version of the reverse TET transactivator (M2rtTA) under regulation of the CAG promoter. When doxycycline binds the tetracycline reverse transactivator (rtTA), its 3D structure changes facilitating binding to the tetracycline responsive element (TRE) leading to the expression of SNCA-A53T-HA. Neomycin (Neo) and puromycine (Puro) resistance genes enable double selection. SA = splice acceptor, 2A = self-splicing protein. (B) Western Blot analysis for total alpha-synuclein in pluripotent iPSCs exposed to doxycycline for 2 days showed that the protein was expressed in an inducible manner. (C) Immunocytochemistry of iPSC neurons (day 60 of differentiation) showing expression of the pan-neuronal filament markers tau and betaIII-tubulin and the synaptic protein synapsin-I in most cells. A subpopulation of GABA positive cells was present as well as a few cells positive for the neuroprogenitor markers nestin. Scale bars. 200 mum. Representative images from three independent neuronal differentiations. (D) Western Blot analysis for tau, betaIII-tubulin and synapsin-I expression in undifferentiated iPSCs (day 0) and iPSC neurons (day 59 of differentiation). Representative blots of three independent neuronal differentiations.
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- Main image
- Experimental details
- 10.1371/journal.pone.0261536.g002 Fig 2 Exogenous fibrils91 seed alpha-synuclein aggregation in iPSC neurons expressing A53T alpha-synuclein. All graphs are shown as mean+-SEM and ****p
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- Experimental details
- 10.1371/journal.pone.0261536.g003 Fig 3 A53T alpha-synuclein seeding can be modulated. All graphs are shown as mean+-SEM, ns = non-significant, *p
