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Alomone Labs tamapin

Blocking SK3 channels in microglia reduces their neurotoxic behavior . Microglia on Transwell™ inserts were incubated with lipopolysaccharide (LPS; 100 ng/ml, 24 h), with or without 100 <t>nM</t> <t>apamin,</t> 5 nM <t>tamapin</t> or 250 pM tamapin. The inserts were then washed to remove the drugs; thus, target neurons were never exposed to LPS or channel blockers. Each microglia-bearing insert was placed in a Transwell™ chamber above healthy neurons, incubated for 24 h (for caspase 3 activation) or 48 h (for TUNEL), and then the target neuron cultures were removed and assessed. Results are presented as mean±SEM for the number of separate cultures indicated on the bars. A . TUNEL-positive neuronal nuclei were counted and expressed as a percentage of all DAPI-stained nuclei. LPS-stimulated microglia killed more neurons than untreated microglia ( †† p < 0.01), and killing was significantly reduced by treating the microglia with 100 nM apamin (* p < 0.05) or 5 nM tamapin (* p < 0.05), but not with 250 pM tamapin. B . Average caspase 3 activity in each neuron-containing well was measured with a fluorogenic substrate (Ac-DEVD-AMC) and the fluorescence plate reader. Treating microglia with either 100 nM apamin or 5 nM tamapin reduced caspase-3 activation in the target neurons (* p < 0.05); whereas, 250 pM tamapin treatment had no effect.

Tamapin, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 90/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/stt-400/pmc02819255-95-10-11?v=Alomone+Labs
Average 90 stars, based on 4 article reviews

tamapin - by Bioz Stars, 2026-07

90/100 stars

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1) Product Images from "The Ca 2+ activated SK3 channel is expressed in microglia in the rat striatum and contributes to microglia-mediated neurotoxicity in vitro"

Article Title: The Ca 2+ activated SK3 channel is expressed in microglia in the rat striatum and contributes to microglia-mediated neurotoxicity in vitro

Journal: Journal of Neuroinflammation

doi: 10.1186/1742-2094-7-4

Figure Legend Snippet: Blocking SK3 channels in microglia reduces their neurotoxic behavior . Microglia on Transwell™ inserts were incubated with lipopolysaccharide (LPS; 100 ng/ml, 24 h), with or without 100 nM apamin, 5 nM tamapin or 250 pM tamapin. The inserts were then washed to remove the drugs; thus, target neurons were never exposed to LPS or channel blockers. Each microglia-bearing insert was placed in a Transwell™ chamber above healthy neurons, incubated for 24 h (for caspase 3 activation) or 48 h (for TUNEL), and then the target neuron cultures were removed and assessed. Results are presented as mean±SEM for the number of separate cultures indicated on the bars. A . TUNEL-positive neuronal nuclei were counted and expressed as a percentage of all DAPI-stained nuclei. LPS-stimulated microglia killed more neurons than untreated microglia ( †† p < 0.01), and killing was significantly reduced by treating the microglia with 100 nM apamin (* p < 0.05) or 5 nM tamapin (* p < 0.05), but not with 250 pM tamapin. B . Average caspase 3 activity in each neuron-containing well was measured with a fluorogenic substrate (Ac-DEVD-AMC) and the fluorescence plate reader. Treating microglia with either 100 nM apamin or 5 nM tamapin reduced caspase-3 activation in the target neurons (* p < 0.05); whereas, 250 pM tamapin treatment had no effect.

Techniques Used: Blocking Assay, Incubation, Activation Assay, TUNEL Assay, Staining, Activity Assay, Fluorescence

Blocking SK3 channels reduces microglial iNOS and NO, and tyrosine nitration of target neurons . Microglia were grown on Transwell™ inserts, and treated with LPS (100 ng/ml, 24 h), with or without 100 nM apamin, 5 nM tamapin or 250 pM tamapin. Results are expressed as RFU/mg protein in each well (mean±SEM; # of cell cultures indicated on bars), normalized to the signal from untreated microglia. A . iNOS protein was monitored with a mouse monoclonal anti-iNOS antibody (1:200) and a Cy3-conjugated secondary antibody (1:500). LPS stimulation increased iNOS expression ( † p < 0.05), which was reduced by 100 nM apamin (* p < 0.05) or 5 nM tamapin (** p < 0.01), but not by 250 pM tamapin. B . Nitric oxide production was measured as nitrite accumulation, using the Griess assay. LPS increased NO production ( † p < 0.05), which was abrogated by 100 nM apamin (** p < 0.01) or 5 nM tamapin (** p < 0.01), but unaffected by 250 pM tamapin. C . Tyrosine nitrated proteins in the target neurons were monitored with a rabbit polyclonal antibody against nitrotyrosine residues (1:200) and Cy3-conjugated secondary antibody. LPS-stimulated microglia induced tyrosine nitration in neurons ( † p < 0.05), and this was abrogated by treating the microglia with 100 nM apamin (*** p < 0.001) or 5 nM tamapin (** p < 0.01), but not by 250 pM tamapin.

Figure Legend Snippet: Blocking SK3 channels reduces microglial iNOS and NO, and tyrosine nitration of target neurons . Microglia were grown on Transwell™ inserts, and treated with LPS (100 ng/ml, 24 h), with or without 100 nM apamin, 5 nM tamapin or 250 pM tamapin. Results are expressed as RFU/mg protein in each well (mean±SEM; # of cell cultures indicated on bars), normalized to the signal from untreated microglia. A . iNOS protein was monitored with a mouse monoclonal anti-iNOS antibody (1:200) and a Cy3-conjugated secondary antibody (1:500). LPS stimulation increased iNOS expression ( † p < 0.05), which was reduced by 100 nM apamin (* p < 0.05) or 5 nM tamapin (** p < 0.01), but not by 250 pM tamapin. B . Nitric oxide production was measured as nitrite accumulation, using the Griess assay. LPS increased NO production ( † p < 0.05), which was abrogated by 100 nM apamin (** p < 0.01) or 5 nM tamapin (** p < 0.01), but unaffected by 250 pM tamapin. C . Tyrosine nitrated proteins in the target neurons were monitored with a rabbit polyclonal antibody against nitrotyrosine residues (1:200) and Cy3-conjugated secondary antibody. LPS-stimulated microglia induced tyrosine nitration in neurons ( † p < 0.05), and this was abrogated by treating the microglia with 100 nM apamin (*** p < 0.001) or 5 nM tamapin (** p < 0.01), but not by 250 pM tamapin.

Techniques Used: Blocking Assay, Nitration, Expressing, Griess Assay

Blocking microglial SK3 channels inhibits p38 MAPK (but not NFκB) activation . Microglia cultures were treated with LPS (100 ng/ml), with or without 100 nM apamin, 5 nM tamapin or 250 pM tamapin. p38 MAPK activation was monitored with a rabbit polyclonal antibody against phosphorylated (active) p38 MAPK (1:50). NF-κB activation was monitored as degradation of IκB-α, using a rabbit polyclonal antibody against IκB-α (1:100). Immunoreactivity was detected using a Cy3-conjugated secondary antibody (1:500). A . The phospho-p38 MAPK fluorescence signal was increased in microglia after 30 min lipopolysaccharide treatment († p < 0.05). This activation was prevented by 100 nM apamin (* p < 0.05) or 5 nM tamapin (* p < 0.05), but not by 250 pM tamapin. C . NF-κB was activated in microglia after 30 min lipopolysaccharide treatment, as judged by the decrease in IκB-α fluorescence ( † p < 0.05). NF-κB activation was not affected by apamin or tamapin.

Figure Legend Snippet: Blocking microglial SK3 channels inhibits p38 MAPK (but not NFκB) activation . Microglia cultures were treated with LPS (100 ng/ml), with or without 100 nM apamin, 5 nM tamapin or 250 pM tamapin. p38 MAPK activation was monitored with a rabbit polyclonal antibody against phosphorylated (active) p38 MAPK (1:50). NF-κB activation was monitored as degradation of IκB-α, using a rabbit polyclonal antibody against IκB-α (1:100). Immunoreactivity was detected using a Cy3-conjugated secondary antibody (1:500). A . The phospho-p38 MAPK fluorescence signal was increased in microglia after 30 min lipopolysaccharide treatment († p < 0.05). This activation was prevented by 100 nM apamin (* p < 0.05) or 5 nM tamapin (* p < 0.05), but not by 250 pM tamapin. C . NF-κB was activated in microglia after 30 min lipopolysaccharide treatment, as judged by the decrease in IκB-α fluorescence ( † p < 0.05). NF-κB activation was not affected by apamin or tamapin.

Techniques Used: Blocking Assay, Activation Assay, Fluorescence

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Journal: Journal of Neuroinflammation

Article Title: The Ca 2+ activated SK3 channel is expressed in microglia in the rat striatum and contributes to microglia-mediated neurotoxicity in vitro

doi: 10.1186/1742-2094-7-4

Figure Lengend Snippet: Blocking SK3 channels in microglia reduces their neurotoxic behavior . Microglia on Transwell™ inserts were incubated with lipopolysaccharide (LPS; 100 ng/ml, 24 h), with or without 100 nM apamin, 5 nM tamapin or 250 pM tamapin. The inserts were then washed to remove the drugs; thus, target neurons were never exposed to LPS or channel blockers. Each microglia-bearing insert was placed in a Transwell™ chamber above healthy neurons, incubated for 24 h (for caspase 3 activation) or 48 h (for TUNEL), and then the target neuron cultures were removed and assessed. Results are presented as mean±SEM for the number of separate cultures indicated on the bars. A . TUNEL-positive neuronal nuclei were counted and expressed as a percentage of all DAPI-stained nuclei. LPS-stimulated microglia killed more neurons than untreated microglia ( †† p < 0.01), and killing was significantly reduced by treating the microglia with 100 nM apamin (* p < 0.05) or 5 nM tamapin (* p < 0.05), but not with 250 pM tamapin. B . Average caspase 3 activity in each neuron-containing well was measured with a fluorogenic substrate (Ac-DEVD-AMC) and the fluorescence plate reader. Treating microglia with either 100 nM apamin or 5 nM tamapin reduced caspase-3 activation in the target neurons (* p < 0.05); whereas, 250 pM tamapin treatment had no effect.

Article Snippet: If apamin affected the function of interest, then 5 nM tamapin (Alomone) was used, which fully blocks SK2 (K d = 24 pM) and significantly blocks SK3 (K d = 1.7 nM) [ ].

Techniques: Blocking Assay, Incubation, Activation Assay, TUNEL Assay, Staining, Activity Assay, Fluorescence

Journal: Journal of Neuroinflammation

Article Title: The Ca 2+ activated SK3 channel is expressed in microglia in the rat striatum and contributes to microglia-mediated neurotoxicity in vitro

doi: 10.1186/1742-2094-7-4

Figure Lengend Snippet: Blocking SK3 channels reduces microglial iNOS and NO, and tyrosine nitration of target neurons . Microglia were grown on Transwell™ inserts, and treated with LPS (100 ng/ml, 24 h), with or without 100 nM apamin, 5 nM tamapin or 250 pM tamapin. Results are expressed as RFU/mg protein in each well (mean±SEM; # of cell cultures indicated on bars), normalized to the signal from untreated microglia. A . iNOS protein was monitored with a mouse monoclonal anti-iNOS antibody (1:200) and a Cy3-conjugated secondary antibody (1:500). LPS stimulation increased iNOS expression ( † p < 0.05), which was reduced by 100 nM apamin (* p < 0.05) or 5 nM tamapin (** p < 0.01), but not by 250 pM tamapin. B . Nitric oxide production was measured as nitrite accumulation, using the Griess assay. LPS increased NO production ( † p < 0.05), which was abrogated by 100 nM apamin (** p < 0.01) or 5 nM tamapin (** p < 0.01), but unaffected by 250 pM tamapin. C . Tyrosine nitrated proteins in the target neurons were monitored with a rabbit polyclonal antibody against nitrotyrosine residues (1:200) and Cy3-conjugated secondary antibody. LPS-stimulated microglia induced tyrosine nitration in neurons ( † p < 0.05), and this was abrogated by treating the microglia with 100 nM apamin (*** p < 0.001) or 5 nM tamapin (** p < 0.01), but not by 250 pM tamapin.

Article Snippet: If apamin affected the function of interest, then 5 nM tamapin (Alomone) was used, which fully blocks SK2 (K d = 24 pM) and significantly blocks SK3 (K d = 1.7 nM) [ ].

Techniques: Blocking Assay, Nitration, Expressing, Griess Assay

Journal: Journal of Neuroinflammation

Article Title: The Ca 2+ activated SK3 channel is expressed in microglia in the rat striatum and contributes to microglia-mediated neurotoxicity in vitro

doi: 10.1186/1742-2094-7-4

Figure Lengend Snippet: Blocking microglial SK3 channels inhibits p38 MAPK (but not NFκB) activation . Microglia cultures were treated with LPS (100 ng/ml), with or without 100 nM apamin, 5 nM tamapin or 250 pM tamapin. p38 MAPK activation was monitored with a rabbit polyclonal antibody against phosphorylated (active) p38 MAPK (1:50). NF-κB activation was monitored as degradation of IκB-α, using a rabbit polyclonal antibody against IκB-α (1:100). Immunoreactivity was detected using a Cy3-conjugated secondary antibody (1:500). A . The phospho-p38 MAPK fluorescence signal was increased in microglia after 30 min lipopolysaccharide treatment († p < 0.05). This activation was prevented by 100 nM apamin (* p < 0.05) or 5 nM tamapin (* p < 0.05), but not by 250 pM tamapin. C . NF-κB was activated in microglia after 30 min lipopolysaccharide treatment, as judged by the decrease in IκB-α fluorescence ( † p < 0.05). NF-κB activation was not affected by apamin or tamapin.

Article Snippet: If apamin affected the function of interest, then 5 nM tamapin (Alomone) was used, which fully blocks SK2 (K d = 24 pM) and significantly blocks SK3 (K d = 1.7 nM) [ ].

Techniques: Blocking Assay, Activation Assay, Fluorescence

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1) Product Images from "The Ca 2+ activated SK3 channel is expressed in microglia in the rat striatum and contributes to microglia-mediated neurotoxicity in vitro"

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