- 35-5200 - Invitrogen Antibodies MAPT antibody

Submitted references Loss of function of the mitochondrial peptidase PITRM1 induces proteotoxic stress and Alzheimer's disease-like pathology in human cerebral organoids.

Pérez MJ, Ivanyuk D, Panagiotakopoulou V, Di Napoli G, Kalb S, Brunetti D, Al-Shaana R, Kaeser SA, Fraschka SA, Jucker M, Zeviani M, Viscomi C, Deleidi M
Molecular psychiatry 2021 Oct;26(10):5733-5750

The Isoquinoline Alkaloid Dauricine Targets Multiple Molecular Pathways to Ameliorate Alzheimer-Like Pathological Changes In Vitro.

Liu P, Chen X, Zhou H, Wang L, Zhang Z, Ren X, Zhu F, Guo Y, Huang X, Liu J, Spencer PS, Yang X
Oxidative medicine and cellular longevity 2018;2018:2025914

Aberrant Wnt signaling pathway in medial temporal lobe structures of Alzheimer's disease.

Riise J, Plath N, Pakkenberg B, Parachikova A
Journal of neural transmission (Vienna, Austria : 1996) 2015 Sep;122(9):1303-18

Deficient hippocampal insulin signaling and augmented Tau phosphorylation is related to obesity- and age-induced peripheral insulin resistance: a study in Zucker rats.

Špolcová A, Mikulášková B, Kršková K, Gajdošechová L, Zórad Š, Olszanecki R, Suski M, Bujak-Giżycka B, Železná B, Maletínská L
BMC neuroscience 2014 Sep 25;15:111

Abnormal serine phosphorylation of insulin receptor substrate 1 is associated with tau pathology in Alzheimer's disease and tauopathies.

Yarchoan M, Toledo JB, Lee EB, Arvanitakis Z, Kazi H, Han LY, Louneva N, Lee VM, Kim SF, Trojanowski JQ, Arnold SE
Acta neuropathologica 2014 Nov;128(5):679-89

Neurological characterization of mice deficient in GSK3α highlight pleiotropic physiological functions in cognition and pathological activity as Tau kinase.

Maurin H, Lechat B, Dewachter I, Ris L, Louis JV, Borghgraef P, Devijver H, Jaworski T, Van Leuven F
Molecular brain 2013 May 25;6:27

Unique Alzheimer's disease paired helical filament specific epitopes involve double phosphorylation at specific sites.

Hoffmann R, Lee VM, Leight S, Varga I, Otvos L Jr
Biochemistry 1997 Jul 1;36(26):8114-24

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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Immunohistochemistry analysis of Tau (pT231) showing staining in the cytoplasm and membrane of paraffin-embedded human brain tissue (right) compared to a negative control without primary antibody (left). To expose target proteins, antigen retrieval was performed using 10 mM sodium citrate (pH 6.0), microwaved for 8-15 min. Following antigen retrieval, tissues were blocked in 3% H2O2-methanol for 15 min at room temperature, washed with ddH2O and PBS, and then probed with Tau (pT231) Monoclonal antibody (Product # 35-5200) diluted in 3% BSA-PBS at a dilution of 1:20 overnight at 4°C in a humidified chamber. Tissues were washed extensively in PBST and detection was performed using a HRP-conjugated secondary antibody followed by colorimetric detection using a DAB kit. Tissues were counterstained with hematoxylin and dehydrated with ethanol and xylene to prep for mounting.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 10 Biochemical analysis of protein Tau in GSK3alpha deficient mice. A . Biochemical analysis by western blotting of total protein extracts from forebrain of AAC and AA- mice aged 3, 6 and 18 months (n=5/age). Tau protein levels are normalized to actin and expressed relative to control AA- mice at age 3 months. Data (mean+-SEM) are statistically analyzed by two-way Anova (Bonferroni post hoc test), genotype: F (1,24) =3.40, p=0.5093; age: F (2,24) =37.60, p=0.0027; interaction: F (2,24) =0.20, p=0.7759. Lower panels show representative western blots. B . Biochemical analysis by western blotting for phospho-epitopes pS396/404, pS199 and pT231 of endogenous mouse Tau in total protein extracts from hippocampus and forebrain of AAC and control AA- mice. C . Biochemical analysis by western blotting for phospho-epitopes pS396/404, pS199 and pT231 of endogenous mouse Tau in total protein extracts from hippocampus and cortex of GSK3alpha.KO and FVB wild-type mice. D . Biochemical analysis by western blotting for phospho-epitopes pS396/404, pS199 and pT231 of human Tau.P301L in total protein extracts from hippocampus and cortex of GSK3alpha.KOxTau.P301L mice and the parental Tau.P301L mice. In panels B-D , all data are normalized for total Tau and reported relative to the respective control mice. Data (mean+-SEM) are statistically analyzed by unpaired Student's t-test (two-tailed), n=6 or 7 per genotype; * p

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 2 Biochemical analysis of GSK3 isozymes in mouse brain extracts. Levels of total GSK3 protein, pS21/S9 and pY279/Y216 in total protein extracts from hippocampus and forebrain from AAC mice compared to control AA- mice ( A ) and from hippocampus and cortex from GSK3alpha.KO mice versus wild-type FvB mice ( B ). Western blots were digitally quantified, normalized for actin and reported relative to the respective control mice. Data (mean+-SEM) are statistically analyzed by unpaired Student's t-test (two-tailed), n=6 or 7 per genotype; *p

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 3 Hyperphosphorylation of Tau protein on different epitopes in hippocampi of fa/fa rats and their control. A Western blots of phosphorylation of Tau protein on the epitopes Ser396 and Thr231 (n = 6 rats per group) B Densitometric quantification of western blots normalized to beta-actin: data are mean +- SD (n = 6 rats per group). Statistical analysis was calculated by two-way ANOVA, Bonferroni post hoc test.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 3 DAU attenuated tau phosphorylation in both N2a/APP cells and HEK293/Tau cells. Levels of phosphorylated tau and total tau in N2a/WT and N2a/APP cells (a, b) and in HEK293/Tau cells (c, d) as determined by Western blot analysis. beta -Actin was used as a loading control. N = 3. Data show the mean +- SEM. * P < 0.05 compared to N2a/WT cells, # P < 0.05 and ## P < 0.01 compared to untreated N2a/APP cells, and & P < 0.05 and &&& P < 0.001 compared to untreated HEK293/Tau cells.

35-5200

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