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milli-mark neuronal antibody cocktail  (Millipore)

 
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    Millipore milli-mark neuronal antibody cocktail
    ( a ) Impact of Nrf2 deficiency on vulnerability to H 2 O 2 treatment, in DIV10 astrocytes <t>(>98%</t> <t>GFAP</t> + astrocytes) or neurons (cortical cultures containing >98% NeuN + neurons, <0.02% GFAP + astrocytes). Cells were treated with H 2 O 2 , fixed after 24 h, DAPI stained and scored for survival/death based on nuclear morphology. * P <0.05, Student's t -test here and throughout unless otherwise stated (neurons: n =4, 700–2000 cells analysed per condition per genotype (PCPG); astrocytes wt n =5, 700–2,000 cells PCPG, ko n =7, 2,100–2,700 cells PCPG). Data are displayed as mean±s.e.m. throughout. ( b ) Nrf2 target genes Cat and Gclc expression analysed by qRT–PCR, normalized to 18s rRNA, expressed relative to the level in pure neuronal cultures. Mixed cultures: approximately 10% GFAP + astrocytes, 90% NeuN + neurons. * P <0.05, Cat n =6, Gclc n =7. ( c , d ) Impact of Nrf2 deficiency on Cat or Gclc mRNA expression in neurons ( c ) and astrocytes ( d ). * P <0.05 compared with wild type (WT); Cat n =4, Gclc n =5. ( e ) qRT–PCR analysis of Nrf2 target gene (Hmox1, Srxn1 and xCT) expression in response to tBHQ (10 μM, 8 h) treatment of neuronal or mixed cultures. * P <0.05 ( n =5–6). ( f ) Immunohistochemical analysis of Hmox1 expression in tBHQ-treated mixed cultures. * P <0.05 ( n =5). Upper: example pictures illustrating elevation of Hmox1 in astrocytes within tBHQ-treated mixed cultures. Scale bar, 25 μm. ( g – i ) The effect of Keap1 deficiency on Nrf2 target genes. * P <0.05 (compared with WT control (Con), n =8–15). ( j ) Nrf2 mRNA analysed in parallel cultures of the indicated types. * P <0.05, ( n =10). ( k ) Western blot analysis of Nrf2 expression in different cell types treated with tBHQ (TB; 10 μM) or MG132 (MG; 5 μM) for 16 h. ( l ) Images of mixed cultures treated as indicated and stained with an anti-Nrf2 antibody (red) and a neuronal marker <t>(Milli-Mark).</t> White arrows highlight lack of Nrf2 induction in neurons. Scale bar, 25 μm. ( m ) qRT–PCR analysis of Nrf2 and neuronal/non-neuronal marker gene expression in RNA isolated from FAC-sorted adult cortical NeuN + neurons, expressed relative to levels in NeuN − cells. * P <0.05 ( n =4). See . ( n ) Expression of NRF2 ( NEF2L2 ) and GRIN1 analysed in astrocytes and neurons derived from H9 hESCs. * P <0.05 ( n =3). NS, not significant.
    Milli Mark Neuronal Antibody Cocktail, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/milli-mark neuronal antibody cocktail/product/Millipore
    Average 90 stars, based on 1 article reviews
    milli-mark neuronal antibody cocktail - by Bioz Stars, 2026-03
    90/100 stars

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    1) Product Images from "Neuronal development is promoted by weakened intrinsic antioxidant defences due to epigenetic repression of Nrf2"

    Article Title: Neuronal development is promoted by weakened intrinsic antioxidant defences due to epigenetic repression of Nrf2

    Journal: Nature Communications

    doi: 10.1038/ncomms8066

    ( a ) Impact of Nrf2 deficiency on vulnerability to H 2 O 2 treatment, in DIV10 astrocytes (>98% GFAP + astrocytes) or neurons (cortical cultures containing >98% NeuN + neurons, <0.02% GFAP + astrocytes). Cells were treated with H 2 O 2 , fixed after 24 h, DAPI stained and scored for survival/death based on nuclear morphology. * P <0.05, Student's t -test here and throughout unless otherwise stated (neurons: n =4, 700–2000 cells analysed per condition per genotype (PCPG); astrocytes wt n =5, 700–2,000 cells PCPG, ko n =7, 2,100–2,700 cells PCPG). Data are displayed as mean±s.e.m. throughout. ( b ) Nrf2 target genes Cat and Gclc expression analysed by qRT–PCR, normalized to 18s rRNA, expressed relative to the level in pure neuronal cultures. Mixed cultures: approximately 10% GFAP + astrocytes, 90% NeuN + neurons. * P <0.05, Cat n =6, Gclc n =7. ( c , d ) Impact of Nrf2 deficiency on Cat or Gclc mRNA expression in neurons ( c ) and astrocytes ( d ). * P <0.05 compared with wild type (WT); Cat n =4, Gclc n =5. ( e ) qRT–PCR analysis of Nrf2 target gene (Hmox1, Srxn1 and xCT) expression in response to tBHQ (10 μM, 8 h) treatment of neuronal or mixed cultures. * P <0.05 ( n =5–6). ( f ) Immunohistochemical analysis of Hmox1 expression in tBHQ-treated mixed cultures. * P <0.05 ( n =5). Upper: example pictures illustrating elevation of Hmox1 in astrocytes within tBHQ-treated mixed cultures. Scale bar, 25 μm. ( g – i ) The effect of Keap1 deficiency on Nrf2 target genes. * P <0.05 (compared with WT control (Con), n =8–15). ( j ) Nrf2 mRNA analysed in parallel cultures of the indicated types. * P <0.05, ( n =10). ( k ) Western blot analysis of Nrf2 expression in different cell types treated with tBHQ (TB; 10 μM) or MG132 (MG; 5 μM) for 16 h. ( l ) Images of mixed cultures treated as indicated and stained with an anti-Nrf2 antibody (red) and a neuronal marker (Milli-Mark). White arrows highlight lack of Nrf2 induction in neurons. Scale bar, 25 μm. ( m ) qRT–PCR analysis of Nrf2 and neuronal/non-neuronal marker gene expression in RNA isolated from FAC-sorted adult cortical NeuN + neurons, expressed relative to levels in NeuN − cells. * P <0.05 ( n =4). See . ( n ) Expression of NRF2 ( NEF2L2 ) and GRIN1 analysed in astrocytes and neurons derived from H9 hESCs. * P <0.05 ( n =3). NS, not significant.
    Figure Legend Snippet: ( a ) Impact of Nrf2 deficiency on vulnerability to H 2 O 2 treatment, in DIV10 astrocytes (>98% GFAP + astrocytes) or neurons (cortical cultures containing >98% NeuN + neurons, <0.02% GFAP + astrocytes). Cells were treated with H 2 O 2 , fixed after 24 h, DAPI stained and scored for survival/death based on nuclear morphology. * P <0.05, Student's t -test here and throughout unless otherwise stated (neurons: n =4, 700–2000 cells analysed per condition per genotype (PCPG); astrocytes wt n =5, 700–2,000 cells PCPG, ko n =7, 2,100–2,700 cells PCPG). Data are displayed as mean±s.e.m. throughout. ( b ) Nrf2 target genes Cat and Gclc expression analysed by qRT–PCR, normalized to 18s rRNA, expressed relative to the level in pure neuronal cultures. Mixed cultures: approximately 10% GFAP + astrocytes, 90% NeuN + neurons. * P <0.05, Cat n =6, Gclc n =7. ( c , d ) Impact of Nrf2 deficiency on Cat or Gclc mRNA expression in neurons ( c ) and astrocytes ( d ). * P <0.05 compared with wild type (WT); Cat n =4, Gclc n =5. ( e ) qRT–PCR analysis of Nrf2 target gene (Hmox1, Srxn1 and xCT) expression in response to tBHQ (10 μM, 8 h) treatment of neuronal or mixed cultures. * P <0.05 ( n =5–6). ( f ) Immunohistochemical analysis of Hmox1 expression in tBHQ-treated mixed cultures. * P <0.05 ( n =5). Upper: example pictures illustrating elevation of Hmox1 in astrocytes within tBHQ-treated mixed cultures. Scale bar, 25 μm. ( g – i ) The effect of Keap1 deficiency on Nrf2 target genes. * P <0.05 (compared with WT control (Con), n =8–15). ( j ) Nrf2 mRNA analysed in parallel cultures of the indicated types. * P <0.05, ( n =10). ( k ) Western blot analysis of Nrf2 expression in different cell types treated with tBHQ (TB; 10 μM) or MG132 (MG; 5 μM) for 16 h. ( l ) Images of mixed cultures treated as indicated and stained with an anti-Nrf2 antibody (red) and a neuronal marker (Milli-Mark). White arrows highlight lack of Nrf2 induction in neurons. Scale bar, 25 μm. ( m ) qRT–PCR analysis of Nrf2 and neuronal/non-neuronal marker gene expression in RNA isolated from FAC-sorted adult cortical NeuN + neurons, expressed relative to levels in NeuN − cells. * P <0.05 ( n =4). See . ( n ) Expression of NRF2 ( NEF2L2 ) and GRIN1 analysed in astrocytes and neurons derived from H9 hESCs. * P <0.05 ( n =3). NS, not significant.

    Techniques Used: Staining, Expressing, Quantitative RT-PCR, Immunohistochemical staining, Western Blot, Marker, Isolation, Derivative Assay



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    milli-mark neuronal antibody cocktail  (Millipore)
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    Millipore milli-mark neuronal antibody cocktail
    ( a ) Impact of Nrf2 deficiency on vulnerability to H 2 O 2 treatment, in DIV10 astrocytes <t>(>98%</t> <t>GFAP</t> + astrocytes) or neurons (cortical cultures containing >98% NeuN + neurons, <0.02% GFAP + astrocytes). Cells were treated with H 2 O 2 , fixed after 24 h, DAPI stained and scored for survival/death based on nuclear morphology. * P <0.05, Student's t -test here and throughout unless otherwise stated (neurons: n =4, 700–2000 cells analysed per condition per genotype (PCPG); astrocytes wt n =5, 700–2,000 cells PCPG, ko n =7, 2,100–2,700 cells PCPG). Data are displayed as mean±s.e.m. throughout. ( b ) Nrf2 target genes Cat and Gclc expression analysed by qRT–PCR, normalized to 18s rRNA, expressed relative to the level in pure neuronal cultures. Mixed cultures: approximately 10% GFAP + astrocytes, 90% NeuN + neurons. * P <0.05, Cat n =6, Gclc n =7. ( c , d ) Impact of Nrf2 deficiency on Cat or Gclc mRNA expression in neurons ( c ) and astrocytes ( d ). * P <0.05 compared with wild type (WT); Cat n =4, Gclc n =5. ( e ) qRT–PCR analysis of Nrf2 target gene (Hmox1, Srxn1 and xCT) expression in response to tBHQ (10 μM, 8 h) treatment of neuronal or mixed cultures. * P <0.05 ( n =5–6). ( f ) Immunohistochemical analysis of Hmox1 expression in tBHQ-treated mixed cultures. * P <0.05 ( n =5). Upper: example pictures illustrating elevation of Hmox1 in astrocytes within tBHQ-treated mixed cultures. Scale bar, 25 μm. ( g – i ) The effect of Keap1 deficiency on Nrf2 target genes. * P <0.05 (compared with WT control (Con), n =8–15). ( j ) Nrf2 mRNA analysed in parallel cultures of the indicated types. * P <0.05, ( n =10). ( k ) Western blot analysis of Nrf2 expression in different cell types treated with tBHQ (TB; 10 μM) or MG132 (MG; 5 μM) for 16 h. ( l ) Images of mixed cultures treated as indicated and stained with an anti-Nrf2 antibody (red) and a neuronal marker <t>(Milli-Mark).</t> White arrows highlight lack of Nrf2 induction in neurons. Scale bar, 25 μm. ( m ) qRT–PCR analysis of Nrf2 and neuronal/non-neuronal marker gene expression in RNA isolated from FAC-sorted adult cortical NeuN + neurons, expressed relative to levels in NeuN − cells. * P <0.05 ( n =4). See . ( n ) Expression of NRF2 ( NEF2L2 ) and GRIN1 analysed in astrocytes and neurons derived from H9 hESCs. * P <0.05 ( n =3). NS, not significant.
    Milli Mark Neuronal Antibody Cocktail, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/milli-mark neuronal antibody cocktail/product/Millipore
    Average 90 stars, based on 1 article reviews
    milli-mark neuronal antibody cocktail - by Bioz Stars, 2026-03
    90/100 stars
    		  Buy from Supplier

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    ( a ) Impact of Nrf2 deficiency on vulnerability to H 2 O 2 treatment, in DIV10 astrocytes (>98% GFAP + astrocytes) or neurons (cortical cultures containing >98% NeuN + neurons, <0.02% GFAP + astrocytes). Cells were treated with H 2 O 2 , fixed after 24 h, DAPI stained and scored for survival/death based on nuclear morphology. * P <0.05, Student's t -test here and throughout unless otherwise stated (neurons: n =4, 700–2000 cells analysed per condition per genotype (PCPG); astrocytes wt n =5, 700–2,000 cells PCPG, ko n =7, 2,100–2,700 cells PCPG). Data are displayed as mean±s.e.m. throughout. ( b ) Nrf2 target genes Cat and Gclc expression analysed by qRT–PCR, normalized to 18s rRNA, expressed relative to the level in pure neuronal cultures. Mixed cultures: approximately 10% GFAP + astrocytes, 90% NeuN + neurons. * P <0.05, Cat n =6, Gclc n =7. ( c , d ) Impact of Nrf2 deficiency on Cat or Gclc mRNA expression in neurons ( c ) and astrocytes ( d ). * P <0.05 compared with wild type (WT); Cat n =4, Gclc n =5. ( e ) qRT–PCR analysis of Nrf2 target gene (Hmox1, Srxn1 and xCT) expression in response to tBHQ (10 μM, 8 h) treatment of neuronal or mixed cultures. * P <0.05 ( n =5–6). ( f ) Immunohistochemical analysis of Hmox1 expression in tBHQ-treated mixed cultures. * P <0.05 ( n =5). Upper: example pictures illustrating elevation of Hmox1 in astrocytes within tBHQ-treated mixed cultures. Scale bar, 25 μm. ( g – i ) The effect of Keap1 deficiency on Nrf2 target genes. * P <0.05 (compared with WT control (Con), n =8–15). ( j ) Nrf2 mRNA analysed in parallel cultures of the indicated types. * P <0.05, ( n =10). ( k ) Western blot analysis of Nrf2 expression in different cell types treated with tBHQ (TB; 10 μM) or MG132 (MG; 5 μM) for 16 h. ( l ) Images of mixed cultures treated as indicated and stained with an anti-Nrf2 antibody (red) and a neuronal marker (Milli-Mark). White arrows highlight lack of Nrf2 induction in neurons. Scale bar, 25 μm. ( m ) qRT–PCR analysis of Nrf2 and neuronal/non-neuronal marker gene expression in RNA isolated from FAC-sorted adult cortical NeuN + neurons, expressed relative to levels in NeuN − cells. * P <0.05 ( n =4). See . ( n ) Expression of NRF2 ( NEF2L2 ) and GRIN1 analysed in astrocytes and neurons derived from H9 hESCs. * P <0.05 ( n =3). NS, not significant.

    Journal: Nature Communications

    Article Title: Neuronal development is promoted by weakened intrinsic antioxidant defences due to epigenetic repression of Nrf2

    doi: 10.1038/ncomms8066

    Figure Lengend Snippet: ( a ) Impact of Nrf2 deficiency on vulnerability to H 2 O 2 treatment, in DIV10 astrocytes (>98% GFAP + astrocytes) or neurons (cortical cultures containing >98% NeuN + neurons, <0.02% GFAP + astrocytes). Cells were treated with H 2 O 2 , fixed after 24 h, DAPI stained and scored for survival/death based on nuclear morphology. * P <0.05, Student's t -test here and throughout unless otherwise stated (neurons: n =4, 700–2000 cells analysed per condition per genotype (PCPG); astrocytes wt n =5, 700–2,000 cells PCPG, ko n =7, 2,100–2,700 cells PCPG). Data are displayed as mean±s.e.m. throughout. ( b ) Nrf2 target genes Cat and Gclc expression analysed by qRT–PCR, normalized to 18s rRNA, expressed relative to the level in pure neuronal cultures. Mixed cultures: approximately 10% GFAP + astrocytes, 90% NeuN + neurons. * P <0.05, Cat n =6, Gclc n =7. ( c , d ) Impact of Nrf2 deficiency on Cat or Gclc mRNA expression in neurons ( c ) and astrocytes ( d ). * P <0.05 compared with wild type (WT); Cat n =4, Gclc n =5. ( e ) qRT–PCR analysis of Nrf2 target gene (Hmox1, Srxn1 and xCT) expression in response to tBHQ (10 μM, 8 h) treatment of neuronal or mixed cultures. * P <0.05 ( n =5–6). ( f ) Immunohistochemical analysis of Hmox1 expression in tBHQ-treated mixed cultures. * P <0.05 ( n =5). Upper: example pictures illustrating elevation of Hmox1 in astrocytes within tBHQ-treated mixed cultures. Scale bar, 25 μm. ( g – i ) The effect of Keap1 deficiency on Nrf2 target genes. * P <0.05 (compared with WT control (Con), n =8–15). ( j ) Nrf2 mRNA analysed in parallel cultures of the indicated types. * P <0.05, ( n =10). ( k ) Western blot analysis of Nrf2 expression in different cell types treated with tBHQ (TB; 10 μM) or MG132 (MG; 5 μM) for 16 h. ( l ) Images of mixed cultures treated as indicated and stained with an anti-Nrf2 antibody (red) and a neuronal marker (Milli-Mark). White arrows highlight lack of Nrf2 induction in neurons. Scale bar, 25 μm. ( m ) qRT–PCR analysis of Nrf2 and neuronal/non-neuronal marker gene expression in RNA isolated from FAC-sorted adult cortical NeuN + neurons, expressed relative to levels in NeuN − cells. * P <0.05 ( n =4). See . ( n ) Expression of NRF2 ( NEF2L2 ) and GRIN1 analysed in astrocytes and neurons derived from H9 hESCs. * P <0.05 ( n =3). NS, not significant.

    Article Snippet: Employed primary antibodies include: rabbit anti-Hmox1 (1:1,000, Stressgen Biotechnologies), mouse anti-GFAP (1:400, Sigma), rabbit anti-GFP (1:750, Life Technologies Ltd), Milli-Mark neuronal antibody cocktail (Millipore, 1:500) and Anti-Nrf2 (Cell Signaling).

    Techniques: Staining, Expressing, Quantitative RT-PCR, Immunohistochemical staining, Western Blot, Marker, Isolation, Derivative Assay