Kn 92

Manufactured by Merck Group

Sourced in United States, Germany

The KN-92 is a laboratory equipment product by Merck Group. It is a general-purpose laboratory instrument used for various experimental and analytical tasks. The core function of the KN-92 is to provide a controlled and consistent environment for sample preparation, processing, and analysis.

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Lab products found in correlation

Kn 93, by Merck Group (9 mentions) Nifedipine, by Merck Group (2 mentions) Bapta, by Merck Group (2 mentions) ω conotoxin mviic, by Bio-Techne (2 mentions) Anti vgat oyster550 antibody, by Synaptic Systems (2 mentions) Dpni caged gaba, by Bio-Techne (2 mentions) Rhod 2 tripotassium salt, by AAT Bioquest (2 mentions) ω conotoxin gvia, by Bio-Techne (2 mentions) Anti ha antibody, by Roche (2 mentions) Bicuculline, by Merck Group (2 mentions) Glutamic acid, by Merck Group (1 mentions) Polyethylenimine (pei), by Merck Group (1 mentions) Poly d lysine, by Merck Group (1 mentions) Glycine, by Merck Group (1 mentions) Vectashield hardset mounting medium, by Vector Laboratories (1 mentions) γ 32p atp, by PerkinElmer (1 mentions) Sto 609 acetate, by Cayman Chemical (1 mentions) Dimethyl sulfoxide (dmso), by Thermo Fisher Scientific (1 mentions) Mni caged l glutamate, by Bio-Techne (1 mentions) L name, by Merck Group (1 mentions)

9 protocols using kn 92

Molecular Tools for Neurotransmitter Studies

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Glutamic acid, glycine, polyethylenimine (PEI), poly-D-lysine (PDL) and DL-threo-β-benzyoxyaspartate (TBOA) were purchased from Sigma. Vectashield Hard-Set mounting medium was obtained from Vector Laboratories (Burlingame, CA) while Prolong Gold Antifade with DAPI mounting media (Molecular Probes) was purchased from Thermo Fisher Scientific (Florence, KY). 2-Amino-5,6,7,8-tetrahydro-4-(4-methoxyphenyl)-7-(naphthalen-1-yl)-5-oxo-4H-chromene-3-carbonitrile (UCPH-101) was obtained from Abcam. Tat-CN21 (YGRKKRRQRRKRPPKLGQIGRSKRVVIEDDR) and tat-CN21 Ala (YGRKKRRQRRKAPAKAAQAAASKRVVIEDDR) were synthesized by Biopeptide Co. Inc (San Diego, CA). KN-92 and KN-93 were purchased from EMD Millipore. Radiolabeled [³H]-glutamate was obtained from American Radiolabeled Chemicals and [γ-³²P]-ATP was obtained from Perkin-Elmer.

Chawla A.R., Johnson D.E., Zybura A.S., Leeds B.P., Nelson R.M, & Hudmon A. (2017). Constitutive Regulation of the Glutamate/Aspartate Transporter EAAT1 by Calcium/Calmodulin-Dependent Protein Kinase II. Journal of neurochemistry, 140(3), 421-434.

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Axon Regeneration Inhibitor Evaluation

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All test substances were introduced into DPBS −/− prior to axon transection. All cells were exposed to the test substance(s) in Ca²⁺-free DPBS −/− for 7 minutes, during which cells were transected, before adding Ca²⁺-containing DPBS +/+ and no test substance(s). These test substances included tatCN21 (5 μM), tatSCR (5 μM), KN-93 (20 μM), KN-92 (20 μM) (EMD Millipore, Billerica, MA, US), STO-609 acetate (5 μM, Cayman Chemical, Ann Arbor, MI, US), and DMSO (90 μM and 28 mM, Fisher Scientific, Fair Lawn, NJ). To assist solvation, stock solutions of KN-93, KN-92 and STO-609 were dissolved in DMSO and diluted in DPBS −/−, resulting in a final DMSO concentration of 28 mM (0.2% v/v).

Poon A.D., McGill S.H., Sunkesula S.R., Burgess Z.S., Dunne P.J., Kang E.E, & Bittner G.D. (2018). Ca2+/calmodulin-dependent protein kinase II and Dimethyl Sulfoxide affect the sealing frequencies of transected hippocampal neurons. Journal of neuroscience research, 96(7), 1208-1222.

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Optogenetic Manipulation of Neuronal Signaling

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Anti-vGAT-Oyster 550 antibody was purchased from Synaptic System (Goettingen, Germany). Anti-HA antibody was from Roche (Milan, Italy). BAPTA (1,2-bis(o-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid), L-NAME (L-NG-Nitroarginine methyl ester), Nifedipine (1,4-Dihydro-2,6-dimethyl-4-(2-nitrophenyl)-3,5-pyridinedicarboxylic acid dimethylester), and Bicuculline were purchased from Sigma (Milan, Italy). KN-93 and KN-92 were acquired from Millipore Merck (Darmstadt, Germany). APV (D-(−)-2-Amino-5-phosphonopentanoic acid), CNQX (6-Cyano-7-nitroquinoxaline-2,3-dione), ω-conotoxin MVIIC, ω-conotoxin GVIA, DPNI-caged-GABA (1-(4-Aminobutanoyl)-4-[1,3-bis(dihydroxyphosphoryloxy)propan-2-yloxy]-7-nitroindoline) and MNI-caged-L-glutamate ((S)-α-amino-2,3-dihydro-4-methoxy-7-nitro-δ-oxo-1H-indole-1-pentanoic acid) were purchased from Tocris (Bristol, UK). Rhod-2 tripotassium salt was purchased from AAT Bioquest (Sunnyvale, CA, USA).

Ravasenga T., Ruben M., Regio V., Polenghi A., Petrini E.M, & Barberis A. (2022). Spatial regulation of coordinated excitatory and inhibitory synaptic plasticity at dendritic synapses. Cell Reports, 38(6), 110347.

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Immunochemicals for Neurophysiology Experiments

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Anti-vGAT-Oyster 550 antibody was purchased from Synaptic System (Goettingen, Germany).
Anti-HA antibody was from Roche (Milan, Italy). BAPTA (1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid), L-NAME (L-NG-Nitroarginine methyl ester), Nifedipine (1,4-Dihydro-2,6-dimethyl-4-(2-nitrophenyl)-3,5-pyridinedicarboxylic acid dimethylester), and Bicuculline were purchased from Sigma (Milan, Italy). KN-93 and KN-92 were acquired from Millipore Merck (Darmstadt, Germany). APV (D-(-)-2-Amino-5-phosphonopentanoic acid), CNQX (6-Cyano-7nitroquinoxaline-2,3-dione), ω-conotoxin MVIIC, ω-conotoxin GVIA, DPNI-caged-GABA (1-(4-Aminobutanoyl)-4-[1,3-bis(dihydroxyphosphoryloxy)propan-2-yloxy]-7-nitroindoline) and MNIcaged-L-glutamate ((S)-α-amino-2,3-dihydro-4-methoxy-7-nitro-δ-oxo-1H-indole-1-pentanoic acid) were purchased from Tocris (Bristol, UK). Rhod-2 tripotassium salt was purchased from AAT Bioquest (Sunnyvale, CA, USA).

Ravasenga T., Ruben M., Polenghi A., Petrini E.M., & Barberis A. (2021). Spatial regulation of coordinated excitatory and inhibitory synaptic plasticity at dendritic synapses.

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Cardiac Ion Channel Modulation Protocol

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ATX-II and tetrodotoxin were purchased from Alomone Labs and Tocris Bioscience, respectively. Dithiothreitol (DTT) and coenzyme Q10 (CoQ10) were purchased from Sigma Chemical. The CaMKII inhibitor KN-93 and its inactive analog KN-92 were purchased from EMD Millipore. Ranolazine and the selective I_NaL blocker GS-967 [23 (link)] were provided by Gilead Sciences. The sources of fluorescent dyes and antibodies are indicated in the relevant sections below.

Viatchenko-Karpinski S., Kornyeyev D., El-Bizri N., Budas G., Fan P., Jiang Z., Yang J., Anderson M.E., Shryock J.C., Chang C.P., Belardinelli L, & Yao L. (2014). Intracellular Na+ Overload Causes Oxidation of CaMKII and leads to Ca2+ Mishandling in Isolated Ventricular Myocytes. Journal of molecular and cellular cardiology, 0, 247-256.

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Chondrocyte Isolation and Culture

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Bovine chondrocytes were isolated from metatarsal joints obtained from a local abattoir within 24 h from death. Experiments were performed when primary chondrocytes reached 80% confluence (passage 0, P0) as previously described^{18 (link)}. C3H/10T1/2 cells (ATCC) were cultured according to the manufacturer’s instructions.
Murine femoral heads and patellae were explanted from 1 month-old male 129/Sv mice and processed for gene expression analysis (see below).
If not differently indicated, cells were stimulated in complete medium (DMEM/F-12 1:1 plus GlutaMax, 10% FBS, 1 mM sodium pyruvate, and 2% antibiotic antimycotic solution ThermoFisher Scientific) supplemented with human recombinant WNT3A (100 ng/ml; R&D), DKK1 (100 ng/ml, R&D), IL1B (20 ng/ml; InvivoGen), KN93 or its inactive control KN92 (10 μM; EMD Millipore), Autocamtide-2 related inhibitory peptide II, AIP, 5 μM; Calbiochem) or respective vehicles as indicated.

Nalesso G., Thorup A.S., Eldridge S.E., De Palma A., Kaur A., Peddireddi K., Blighe K., Rana S., Stott B., Vincent T.L., Thomas B.L., Bertrand J., Sherwood J., Fioravanti A., Pitzalis C, & Dell’Accio F. (2021). Calcium calmodulin kinase II activity is required for cartilage homeostasis in osteoarthritis. Scientific Reports, 11, 5682.

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Pharmacological Modulation of Signaling

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Acetylcholine (ACh), PMA and Chelerythrine Cl⁻ were purchased from Sigma-Aldrich. PD150606 was purchased from Tocris. KN-92 and KN-93 were purchased from EMD Millipore. U0126 was purchased from Promega. Drugs were dissolved into DMSO, and 0.1% DMSO vehicle controls were performed for all experiments.

Getz A.M., Visser F., Bell E.M., Xu F., Flynn N.M., Zaidi W, & Syed N.I. (2016). Two proteolytic fragments of menin coordinate the nuclear transcription and postsynaptic clustering of neurotransmitter receptors during synaptogenesis between Lymnaea neurons. Scientific Reports, 6, 31779.

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Mitochondrial Regulation Assays

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ISO, CsA, CGP 20712A (CGP), ICI-118,551 (ICI), PKA inhibitor fragment 14–22 (PKI), RP-8-PIP-CAMPS (8-RP-cAMPs), AIP, (±)-propranolol hydrochloride (Prop), Mdivi-1, atractyloside and mitoTEMPO were purchased from Sigma-Aldrich (St Louis, MO, USA). KN93 and KN92 were purchased from Merck Millipore Corporation (La Jolla, CA, USA). The fluorescent dyes, tetramethylrhodamine methyl ester perchlorate (TMRM), Fluo-4 AM, DCFH-DA, MitoSOX red MitoTracker Red CMXRos and MitoTracker Green FM were purchased from Life Technologies (Eugene, OR, USA).

Xu S., Wang P., Zhang H., Gong G., Gutierrez Cortes N., Zhu W., Yoon Y., Tian R, & Wang W. (2016). CaMKII induces permeability transition through Drp1 phosphorylation during chronic β-AR stimulation. Nature Communications, 7, 13189.

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Inhibitors Modulate Hippocampal Proteostasis

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Cordycepin was purchased from R & D Systems (Minneapolis, MN, USA). MLN8237 was from Selleck Chemcials (Houston, TX, USA). KN-93 and KN-92 were obtained from EMD Millipore (Billerica, MA, USA). Stock solutions of all these reagents were prepared in DMSO and were diluted to the final concentrations in ACSF. For these reagents, the same concentration of DMSO alone was used for controls. A membrane-permeant proteasome inhibitor β-lactone (25 μM final; Cayman Chemical, Ann Arbor, MI, USA) was applied to the hippocampal slices after treatment with the individual inhibitors mentioned above.

Dong C., Vashisht A, & Hegde A.N. (2014). Proteasome regulates the mediators of cytoplasmic polyadenylation signaling during late-phase long-term potentiation. Neuroscience letters, 583, 199-204.

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