n simian llc mk2 cells Search Results


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ATCC simian llc mk2 cells
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ATCC n simian llc mk2 cells
N Simian Llc Mk2 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC llc mk2 cells
Llc Mk2 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC simian kidney derived llc mk2 cells
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ATCC llc mk2
Llc Mk2, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC montpellier n a rhesus monkey kidney epithelial llc mk2 american type culture collection
Montpellier N A Rhesus Monkey Kidney Epithelial Llc Mk2 American Type Culture Collection, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Carna Inc inactive mk2
Inactive Mk2, supplied by Carna Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ABclonal Biotechnology mk2
Fig. 8 | The p38 inhibitor improved anterograde mitochondrial transport in cortical neuron axons. A–D SB203580 lowered <t>MK2</t> activation levels, increased kinesin and mitochondrial transport proteins in the striatum. n = 3. E–G Mitochondrial transport was partially restored. Scale bar = 20 μm. n = 10, *p < 0.05, **p < 0.01.
Mk2, supplied by ABclonal Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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91
Santa Cruz Biotechnology mk2 inhibitor iii
Cytotoxic efficacy of <t>MK2</t> inhibitors in glioblastoma cells. ( a ) U87, U87-EGFRvIII, A172, and U251 cells were treated with CMPD1 or MK2i (0.001–200 μ M; 72 h) and AlamarBlue cell viability assay was performed. EC 50 values were calculated by non-linear regression analysis. Data are expressed as mean±S.E.M. from at least <t>three</t> independent experiments. ( b and c ) U87 spheroids were treated with CMPD1 (72 h) and AlamarBlue cell viability assay was performed ( b ). In parallel, spheroids were dispersed and cells were allowed to form colonies for 12–15 days ( c ). Data are expressed as mean±S.E.M. ( n =3; * P <0.05, *** P <0.001, one-way ANOVA followed by Newman–Keuls test). ( d ) U87 cells were incubated with CMPD1 or MK2i (2 h) and cell lysates were analysed with western blotting using indicated antibodies. ( e ) U87 cells were pre-treated with CMPD1 or MK2i (2 h) and stimulated with IL-1 β (10 ng/ml) for 15 min. Cell lysates were analysed with western blotting using indicated antibodies. ( f ) U87 cells were treated with CMPD1 for indicated time and cell lysates analysed with western blotting using indicated antibodies. In ( d – f ), representative images of three independent experiments are shown.
Mk2 Inhibitor Iii, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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BioSemi active two mk2
Cytotoxic efficacy of <t>MK2</t> inhibitors in glioblastoma cells. ( a ) U87, U87-EGFRvIII, A172, and U251 cells were treated with CMPD1 or MK2i (0.001–200 μ M; 72 h) and AlamarBlue cell viability assay was performed. EC 50 values were calculated by non-linear regression analysis. Data are expressed as mean±S.E.M. from at least <t>three</t> independent experiments. ( b and c ) U87 spheroids were treated with CMPD1 (72 h) and AlamarBlue cell viability assay was performed ( b ). In parallel, spheroids were dispersed and cells were allowed to form colonies for 12–15 days ( c ). Data are expressed as mean±S.E.M. ( n =3; * P <0.05, *** P <0.001, one-way ANOVA followed by Newman–Keuls test). ( d ) U87 cells were incubated with CMPD1 or MK2i (2 h) and cell lysates were analysed with western blotting using indicated antibodies. ( e ) U87 cells were pre-treated with CMPD1 or MK2i (2 h) and stimulated with IL-1 β (10 ng/ml) for 15 min. Cell lysates were analysed with western blotting using indicated antibodies. ( f ) U87 cells were treated with CMPD1 for indicated time and cell lysates analysed with western blotting using indicated antibodies. In ( d – f ), representative images of three independent experiments are shown.
Active Two Mk2, supplied by BioSemi, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Verlag GmbH phos-phorylation of tristetraprolin by mk2
Cytotoxic efficacy of <t>MK2</t> inhibitors in glioblastoma cells. ( a ) U87, U87-EGFRvIII, A172, and U251 cells were treated with CMPD1 or MK2i (0.001–200 μ M; 72 h) and AlamarBlue cell viability assay was performed. EC 50 values were calculated by non-linear regression analysis. Data are expressed as mean±S.E.M. from at least <t>three</t> independent experiments. ( b and c ) U87 spheroids were treated with CMPD1 (72 h) and AlamarBlue cell viability assay was performed ( b ). In parallel, spheroids were dispersed and cells were allowed to form colonies for 12–15 days ( c ). Data are expressed as mean±S.E.M. ( n =3; * P <0.05, *** P <0.001, one-way ANOVA followed by Newman–Keuls test). ( d ) U87 cells were incubated with CMPD1 or MK2i (2 h) and cell lysates were analysed with western blotting using indicated antibodies. ( e ) U87 cells were pre-treated with CMPD1 or MK2i (2 h) and stimulated with IL-1 β (10 ng/ml) for 15 min. Cell lysates were analysed with western blotting using indicated antibodies. ( f ) U87 cells were treated with CMPD1 for indicated time and cell lysates analysed with western blotting using indicated antibodies. In ( d – f ), representative images of three independent experiments are shown.
Phos Phorylation Of Tristetraprolin By Mk2, supplied by Verlag GmbH, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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SMAC Corp smac-mimetic
Cytotoxic efficacy of <t>MK2</t> inhibitors in glioblastoma cells. ( a ) U87, U87-EGFRvIII, A172, and U251 cells were treated with CMPD1 or MK2i (0.001–200 μ M; 72 h) and AlamarBlue cell viability assay was performed. EC 50 values were calculated by non-linear regression analysis. Data are expressed as mean±S.E.M. from at least <t>three</t> independent experiments. ( b and c ) U87 spheroids were treated with CMPD1 (72 h) and AlamarBlue cell viability assay was performed ( b ). In parallel, spheroids were dispersed and cells were allowed to form colonies for 12–15 days ( c ). Data are expressed as mean±S.E.M. ( n =3; * P <0.05, *** P <0.001, one-way ANOVA followed by Newman–Keuls test). ( d ) U87 cells were incubated with CMPD1 or MK2i (2 h) and cell lysates were analysed with western blotting using indicated antibodies. ( e ) U87 cells were pre-treated with CMPD1 or MK2i (2 h) and stimulated with IL-1 β (10 ng/ml) for 15 min. Cell lysates were analysed with western blotting using indicated antibodies. ( f ) U87 cells were treated with CMPD1 for indicated time and cell lysates analysed with western blotting using indicated antibodies. In ( d – f ), representative images of three independent experiments are shown.
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Image Search Results


Fig. 8 | The p38 inhibitor improved anterograde mitochondrial transport in cortical neuron axons. A–D SB203580 lowered MK2 activation levels, increased kinesin and mitochondrial transport proteins in the striatum. n = 3. E–G Mitochondrial transport was partially restored. Scale bar = 20 μm. n = 10, *p < 0.05, **p < 0.01.

Journal: NPJ Parkinson's disease

Article Title: Disruption of axonal transport in Parkinson's disease: the role of pathological α-Syn and AMPK/p38 MAPK signaling.

doi: 10.1038/s41531-025-00926-z

Figure Lengend Snippet: Fig. 8 | The p38 inhibitor improved anterograde mitochondrial transport in cortical neuron axons. A–D SB203580 lowered MK2 activation levels, increased kinesin and mitochondrial transport proteins in the striatum. n = 3. E–G Mitochondrial transport was partially restored. Scale bar = 20 μm. n = 10, *p < 0.05, **p < 0.01.

Article Snippet: The antibodies used in western blot were as follows: KIF5B (Abcam, ab5629), KLC1 (Abcam, ab174273), KLC2 (Proteintech, 17668), Miro1 (ABclonal, A5838), MTX1 (Proteintech, 11529), MTX2 (Proteintech, 11610), Dynactin (ABclonal, A1783), DIC (Abcam, ab171964), snapin (Proteintech, 10055), TrkB (CST, Q16620), BDNF (Proteintech, 66292), Erk1/2 (Proteintech, 66192), pErk1/2 (ABclonal, AP0974), Rab7 (ABclonal, A12784), PIKE (Proteintech, 14690), AMPK (CST, 5831S), p-AMPK (CST, 2535S), p38 (CST, 8690S), p-p38 (CST, 4511S), α-synuclein (Abcam, ab212184), α-synuclein pSer129 (Abcam, ab51253), TH (Abcam, ab75875), DAT (Proteintech, 22525), MK2 (ABclonal, A10668), CREB (ABclonal, A11989), p-CREB (ABclonal, AP0903).

Techniques: Activation Assay

Cytotoxic efficacy of MK2 inhibitors in glioblastoma cells. ( a ) U87, U87-EGFRvIII, A172, and U251 cells were treated with CMPD1 or MK2i (0.001–200 μ M; 72 h) and AlamarBlue cell viability assay was performed. EC 50 values were calculated by non-linear regression analysis. Data are expressed as mean±S.E.M. from at least three independent experiments. ( b and c ) U87 spheroids were treated with CMPD1 (72 h) and AlamarBlue cell viability assay was performed ( b ). In parallel, spheroids were dispersed and cells were allowed to form colonies for 12–15 days ( c ). Data are expressed as mean±S.E.M. ( n =3; * P <0.05, *** P <0.001, one-way ANOVA followed by Newman–Keuls test). ( d ) U87 cells were incubated with CMPD1 or MK2i (2 h) and cell lysates were analysed with western blotting using indicated antibodies. ( e ) U87 cells were pre-treated with CMPD1 or MK2i (2 h) and stimulated with IL-1 β (10 ng/ml) for 15 min. Cell lysates were analysed with western blotting using indicated antibodies. ( f ) U87 cells were treated with CMPD1 for indicated time and cell lysates analysed with western blotting using indicated antibodies. In ( d – f ), representative images of three independent experiments are shown.

Journal: Cell Death Discovery

Article Title: Cytotoxic activity of the MK2 inhibitor CMPD1 in glioblastoma cells is independent of MK2

doi: 10.1038/cddiscovery.2015.28

Figure Lengend Snippet: Cytotoxic efficacy of MK2 inhibitors in glioblastoma cells. ( a ) U87, U87-EGFRvIII, A172, and U251 cells were treated with CMPD1 or MK2i (0.001–200 μ M; 72 h) and AlamarBlue cell viability assay was performed. EC 50 values were calculated by non-linear regression analysis. Data are expressed as mean±S.E.M. from at least three independent experiments. ( b and c ) U87 spheroids were treated with CMPD1 (72 h) and AlamarBlue cell viability assay was performed ( b ). In parallel, spheroids were dispersed and cells were allowed to form colonies for 12–15 days ( c ). Data are expressed as mean±S.E.M. ( n =3; * P <0.05, *** P <0.001, one-way ANOVA followed by Newman–Keuls test). ( d ) U87 cells were incubated with CMPD1 or MK2i (2 h) and cell lysates were analysed with western blotting using indicated antibodies. ( e ) U87 cells were pre-treated with CMPD1 or MK2i (2 h) and stimulated with IL-1 β (10 ng/ml) for 15 min. Cell lysates were analysed with western blotting using indicated antibodies. ( f ) U87 cells were treated with CMPD1 for indicated time and cell lysates analysed with western blotting using indicated antibodies. In ( d – f ), representative images of three independent experiments are shown.

Article Snippet: Inhibitors CMPD1 (sc-203138) and MK2 inhibitor III (sc-221948) were from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

Techniques: Viability Assay, Incubation, Western Blot

Effect of MK2 knock-down on viability, cell cycle, and apoptosis in U87 cells. ( a ) U87 cells were reverse-transfected with control or MK2-targeting siRNA (5 nM). Cells were harvested at indicated time and MK2 expression determined with western blotting. Representative images of three independent experiments are shown. ( b ) Cells were transfected as in ( a ) and AlamarBlue cell viability assay was performed 72 h post transfection. Data are expressed as mean±S.E.M. ( n =5; * P <0.05, unpaired t -test). ( c and d ) Cells were transfected as in ( a ), and cell-cycle analysis ( c ) and Annexin-V staining ( d ) were performed 48 h post transfection. Data are expressed as mean±S.E.M. ( n =3). ( e ) U87 cells were transfected as in ( a ) overnight, treated with CMPD1 (72 h) and AlamarBlue cell viability was performed. EC 50 was calculated using Prism 5 GraphPad Software. Data are expressed as mean±S.E.M. ( n =4).

Journal: Cell Death Discovery

Article Title: Cytotoxic activity of the MK2 inhibitor CMPD1 in glioblastoma cells is independent of MK2

doi: 10.1038/cddiscovery.2015.28

Figure Lengend Snippet: Effect of MK2 knock-down on viability, cell cycle, and apoptosis in U87 cells. ( a ) U87 cells were reverse-transfected with control or MK2-targeting siRNA (5 nM). Cells were harvested at indicated time and MK2 expression determined with western blotting. Representative images of three independent experiments are shown. ( b ) Cells were transfected as in ( a ) and AlamarBlue cell viability assay was performed 72 h post transfection. Data are expressed as mean±S.E.M. ( n =5; * P <0.05, unpaired t -test). ( c and d ) Cells were transfected as in ( a ), and cell-cycle analysis ( c ) and Annexin-V staining ( d ) were performed 48 h post transfection. Data are expressed as mean±S.E.M. ( n =3). ( e ) U87 cells were transfected as in ( a ) overnight, treated with CMPD1 (72 h) and AlamarBlue cell viability was performed. EC 50 was calculated using Prism 5 GraphPad Software. Data are expressed as mean±S.E.M. ( n =4).

Article Snippet: Inhibitors CMPD1 (sc-203138) and MK2 inhibitor III (sc-221948) were from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

Techniques: Knockdown, Transfection, Control, Expressing, Western Blot, Viability Assay, Cell Cycle Assay, Staining, Software