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k252a (Tocris)

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Tocris k252a
K252a, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 109 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/k-252a/K+252a/pm41922794-355-4-8
Average 93 stars, based on 109 article reviews

k252a - by Bioz Stars, 2026-10

93/100 stars

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Article Title: Hippocampal SENP3 mediates chronic stress-induced depression-like behaviors by impairing the CREB-BDNF signaling.
Article Snippet: Impaired signaling between cyclic adenosine monophosphate response element binding protein (CREB) and brain-derived neurotrophic factor (BDNF) in the hippocampus is generally considered to be the cause of depression.. The mechanisms underlying the impairment of CREB-BDNF signaling under stress conditions are largely unclear.. Small ubiquitin-like modifier (SUMO) specific peptidase 3 (SENP3) is a molecule that can regulate SUMOylation of target proteins related to synaptic plasticity.

Article Title: Cannabinoid overrides triggers of GABAergic plasticity in vestibular circuits and distorts the development of navigation
Article Snippet: K252a ((9S,10R,12R)-2,3,9,10,11,12-hexahydro-10-hydroxy-9-methyl-1-oxo-9,12-epoxy-1H-diindolo[1,2,3-fg:3′,2',1′-kl]pyrrolo[3,4-i][1,6]benzodiazocine-10-carboxylic acid methyl ester) , Tocris Bioscience 1683/200U , .

Article Title: Protease activated receptor-1 regulates mixed lineage kinase-3 to drive triple-negative breast cancer tumorigenesis.
Article Snippet: The pan MLK inhibitor, CEP-1347, was procured from Tocris Biosciences, Minneapolis, MN.

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Article Title: Reduced SH3RF3 may protect against Alzheimer’s disease by lowering microglial pro-inflammatory responses via modulation of JNK and NFkB signaling
Article Snippet: .. In some experiments, iMGLs were pre-treated with chemical inhibitors or DMSO vehicle for 2 hr before inflammatory stimuli, which included CEP-1347 (100 nM; Tocris), IKK16 (1 uM; Tocris), and NSC23766 (50 uM; EMD Millipore). iMGLs were then treated with either the dsRNA viral mimic poly(I:C) at (25 ug/mL) , oligomerized Aβ42 (5 uM; rPeptide), or vehicle control (dH 2 O or F12 media respectively). .. Recombinant Aβ42 was oligomerized as described previously, and validated via Coomassie blue staining and western blot using the 6E10 antibody (1:1000; BioLegend).

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Suppression of the BDNF/TrkB signaling pathway by K252a can partly reverse the KCC2 downregulation and dysfunction after hypoxia injury. (A) NeuN and KCC2 immunolabeling in the hippocampal CA1 region of MCAO‐R mice, and those pretreated with K252a are depicted in confocal scanning images. Scale bars: 50 μm. (B) Quantitative assessment of membrane KCC2 labeling density in fluorescently labeled cells relative to NeuN (Sham: N = 4, MCAO‐R N = 7, MCAO‐ R + K252a: N = 7). (C) Confocal microscopy images illustrate KCC2 (green) and NeuN (blue‐violet) expression in cultured hippocampal neurons exposed to OGD/R with or without K252a. (Control: N = 23 cells; OGD/R: N = 21 cells; OGD/ R + K252a: N = 32 cells, all from N = 5 cultures). Scale bar: 5 μm. (D) Quantitative assessment of membrane KCC2 in cultured hippocampal neurons. (E) Experimental determination of E GABA recorded by a small‐tip whole‐cell patch clamp is depicted in I‐V plots. (F) Statistical analysis indicates a significant positive shift in E GABA after MCAO‐R, which is partially reversed by K252a (MCAO‐ R + K252a: −55.0 ± 4.2 mV, N = 3, n = 21 vs. MCAO‐R: −52.1 ± 3.8 mV, N = 3, n = 15, p = 0.08; MCAO‐ R + K252a vs. Sham: −57.5 ± 3.6 mV, N = 4, n = 19, p = 0.12). (G) Patch clamp recordings using a low‐chloride electrode solution demonstrate that both the amplitude (H) and frequency (I) of mIPSCs, which are KCC2‐dependent, are significantly reduced by MCAO‐R, with only the amplitude being partially rescued by pretreatment with K252a (MCAO‐R: 17.0 ± 3.4 pA, N = 3, n = 17 vs. MCAO‐ R + K252a:19.3 ± 2.8 pA, N = 3, n = 18, p = 0.13; MCAO‐R + K252a vs. Sham:21.3 ± 3.3 pA, N = 3, n = 15). * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the Sham group; ## p < 0.01 and ### p < 0.001 compared to the MCAO‐R group or OGD/R group.

Journal: CNS Neuroscience & Therapeutics

Article Title: KCC2 Dysfunction Mediated by Microglial BDNF / TrkB Signaling Exacerbates Early Post‐Stroke Seizure Susceptibility

doi: 10.1002/cns.70795

Figure Lengend Snippet: Suppression of the BDNF/TrkB signaling pathway by K252a can partly reverse the KCC2 downregulation and dysfunction after hypoxia injury. (A) NeuN and KCC2 immunolabeling in the hippocampal CA1 region of MCAO‐R mice, and those pretreated with K252a are depicted in confocal scanning images. Scale bars: 50 μm. (B) Quantitative assessment of membrane KCC2 labeling density in fluorescently labeled cells relative to NeuN (Sham: N = 4, MCAO‐R N = 7, MCAO‐ R + K252a: N = 7). (C) Confocal microscopy images illustrate KCC2 (green) and NeuN (blue‐violet) expression in cultured hippocampal neurons exposed to OGD/R with or without K252a. (Control: N = 23 cells; OGD/R: N = 21 cells; OGD/ R + K252a: N = 32 cells, all from N = 5 cultures). Scale bar: 5 μm. (D) Quantitative assessment of membrane KCC2 in cultured hippocampal neurons. (E) Experimental determination of E GABA recorded by a small‐tip whole‐cell patch clamp is depicted in I‐V plots. (F) Statistical analysis indicates a significant positive shift in E GABA after MCAO‐R, which is partially reversed by K252a (MCAO‐ R + K252a: −55.0 ± 4.2 mV, N = 3, n = 21 vs. MCAO‐R: −52.1 ± 3.8 mV, N = 3, n = 15, p = 0.08; MCAO‐ R + K252a vs. Sham: −57.5 ± 3.6 mV, N = 4, n = 19, p = 0.12). (G) Patch clamp recordings using a low‐chloride electrode solution demonstrate that both the amplitude (H) and frequency (I) of mIPSCs, which are KCC2‐dependent, are significantly reduced by MCAO‐R, with only the amplitude being partially rescued by pretreatment with K252a (MCAO‐R: 17.0 ± 3.4 pA, N = 3, n = 17 vs. MCAO‐ R + K252a:19.3 ± 2.8 pA, N = 3, n = 18, p = 0.13; MCAO‐R + K252a vs. Sham:21.3 ± 3.3 pA, N = 3, n = 15). * p < 0.05, ** p < 0.01, and *** p < 0.001 compared to the Sham group; ## p < 0.01 and ### p < 0.001 compared to the MCAO‐R group or OGD/R group.

Article Snippet: FUR was purchased from Sigma‐Aldrich, and minocycline, K252a, and CLP290 were from MedChemExpress.

Techniques: Immunolabeling, Membrane, Labeling, Confocal Microscopy, Expressing, Cell Culture, Control, Patch Clamp

Alleviating the severity of MCAO‐R‐induced seizures by blocking the BDNF/TrkB signaling and suppressing microglial activation. (A) Representative traces demonstrate the effective suppression of epileptiform burst firing induced by OGD/R in cultured hippocampal neurons by K252a. (B–D) Bar graphs present quantitative analysis, indicating that blocking the BDNF/TrkB signaling pathway with K252a significantly reduces the percentage of neurons exhibiting epileptiform bursting firing (B), the bursting frequency (C), and the total number of APs during 10 min (D) compared to control neurons (Control: N = 18 cells, OGD/R: N = 24 cells; FUR+OGD/R: N = 11 cells, all from N = 3 cultures). (E, F) Pretreatment with K252a or minocycline significantly decreases the occurrence of Racine IV‐V seizures at 40 mg/kg (E) and 50 mg/kg (F) cumulative PTZ dose. The distribution of seizure scores among mice is represented by the R2, R3, R4, and R5. (G‐H) Line charts reveal that K252a or minocycline reduced the percentage of MCAO‐R mice with Racine IV‐V seizures (G) and the average seizure score (H) at a cumulative PTZ dose of 40 and 50 mg/kg. (I) The cumulative PTZ dose required to induce epileptic behaviors with a Racine IV‐V is increased by blocking the BDNF/TrkB signaling pathway and suppressing microglial activation (Sham: N = 10, MCAO‐R: N = 13, MCAO‐ R + K252a: N = 11, MCAO‐R + Mino: N = 10). (J) Simplified schematic summarizing that MCAO‐R induces microglial activation (↑Iba1) and BDNF release, leading to TrkB activation, KCC2 downregulation, a depolarizing shift in E GABA and increased seizure risk, whereas minocycline and K252a act upstream at microglia and TrkB, respectively, to ameliorate this cascade. * p < 0.05 and ** p < 0.01 compared to the Sham group; # p < 0.05 and ## p < 0.01 compared to the MCAO‐R group.

Journal: CNS Neuroscience & Therapeutics

Article Title: KCC2 Dysfunction Mediated by Microglial BDNF / TrkB Signaling Exacerbates Early Post‐Stroke Seizure Susceptibility

doi: 10.1002/cns.70795

Figure Lengend Snippet: Alleviating the severity of MCAO‐R‐induced seizures by blocking the BDNF/TrkB signaling and suppressing microglial activation. (A) Representative traces demonstrate the effective suppression of epileptiform burst firing induced by OGD/R in cultured hippocampal neurons by K252a. (B–D) Bar graphs present quantitative analysis, indicating that blocking the BDNF/TrkB signaling pathway with K252a significantly reduces the percentage of neurons exhibiting epileptiform bursting firing (B), the bursting frequency (C), and the total number of APs during 10 min (D) compared to control neurons (Control: N = 18 cells, OGD/R: N = 24 cells; FUR+OGD/R: N = 11 cells, all from N = 3 cultures). (E, F) Pretreatment with K252a or minocycline significantly decreases the occurrence of Racine IV‐V seizures at 40 mg/kg (E) and 50 mg/kg (F) cumulative PTZ dose. The distribution of seizure scores among mice is represented by the R2, R3, R4, and R5. (G‐H) Line charts reveal that K252a or minocycline reduced the percentage of MCAO‐R mice with Racine IV‐V seizures (G) and the average seizure score (H) at a cumulative PTZ dose of 40 and 50 mg/kg. (I) The cumulative PTZ dose required to induce epileptic behaviors with a Racine IV‐V is increased by blocking the BDNF/TrkB signaling pathway and suppressing microglial activation (Sham: N = 10, MCAO‐R: N = 13, MCAO‐ R + K252a: N = 11, MCAO‐R + Mino: N = 10). (J) Simplified schematic summarizing that MCAO‐R induces microglial activation (↑Iba1) and BDNF release, leading to TrkB activation, KCC2 downregulation, a depolarizing shift in E GABA and increased seizure risk, whereas minocycline and K252a act upstream at microglia and TrkB, respectively, to ameliorate this cascade. * p < 0.05 and ** p < 0.01 compared to the Sham group; # p < 0.05 and ## p < 0.01 compared to the MCAO‐R group.

Article Snippet: FUR was purchased from Sigma‐Aldrich, and minocycline, K252a, and CLP290 were from MedChemExpress.

Techniques: Blocking Assay, Activation Assay, Cell Culture, Control

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