hin diii digested lambda dna Search Results


lambda dna- hin diii dna size marker  (Promega)
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Promega lambda dna- hin diii dna size marker
14,15-EET exerts its antiapoptotic effects in LLCPKcl4 cells by activation of a PI-3 kinase–Akt-signaling pathway. (A) 14,15-EET's antiapoptotic effects were abolished by inhibition of PI-3 kinase but not by inhibition of MAP kinase. After pretreatment with or without the specific PI-3 kinase inhibitor wortmannin (10 nM) or LY294002 (5 μM) or the MEK inhibitor PD98059 (10 μM) for 30 min, followed by 14,15-EET or vehicle for 1 h, LLCPKcl4 cells were exposed to H2O2 for 24 h, and <t>DNA</t> laddering was assessed. (B) Arachidonic acid's antiapoptotic effects in BM3 cells were abolished by inhibition of PI-3 kinase but not by inhibition of MAP kinase. Before induction of H2O2-mediated apoptosis, BM3 cells were pretreated with or without wortmannin, LY294002, or PD98059 and then treated with or without arachidonic acid. (A and B) Leftmost lane, 100-bp DNA ladder; rightmost lane, <t>lambda</t> DNA-HindIII size marker. (C) 14,15-EET increased Akt kinase activity, which was abolished by either wortmannin or LY294002. After treatment with or without the specific PI-3 kinase inhibitor wortmannin (10 nM) or LY294002 (5 μM), LLCPKcl4 cells were treated with or without 14,15-EET. The cells were then lysed and subjected to immunoprecipitation and Akt kinase activity assay with histone H2B as a substrate.
Lambda Dna Hin Diii Dna Size Marker, supplied by Promega, 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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14,15-EET exerts its antiapoptotic effects in LLCPKcl4 cells by activation of a PI-3 kinase–Akt-signaling pathway. (A) 14,15-EET's antiapoptotic effects were abolished by inhibition of PI-3 kinase but not by inhibition of MAP kinase. After pretreatment with or without the specific PI-3 kinase inhibitor wortmannin (10 nM) or LY294002 (5 μM) or the MEK inhibitor PD98059 (10 μM) for 30 min, followed by 14,15-EET or vehicle for 1 h, LLCPKcl4 cells were exposed to H2O2 for 24 h, and DNA laddering was assessed. (B) Arachidonic acid's antiapoptotic effects in BM3 cells were abolished by inhibition of PI-3 kinase but not by inhibition of MAP kinase. Before induction of H2O2-mediated apoptosis, BM3 cells were pretreated with or without wortmannin, LY294002, or PD98059 and then treated with or without arachidonic acid. (A and B) Leftmost lane, 100-bp DNA ladder; rightmost lane, lambda DNA-HindIII size marker. (C) 14,15-EET increased Akt kinase activity, which was abolished by either wortmannin or LY294002. After treatment with or without the specific PI-3 kinase inhibitor wortmannin (10 nM) or LY294002 (5 μM), LLCPKcl4 cells were treated with or without 14,15-EET. The cells were then lysed and subjected to immunoprecipitation and Akt kinase activity assay with histone H2B as a substrate.

Journal:

Article Title: Cytochrome P450 Epoxygenase Metabolism of Arachidonic Acid Inhibits Apoptosis

doi: 10.1128/MCB.21.18.6322-6331.2001

Figure Lengend Snippet: 14,15-EET exerts its antiapoptotic effects in LLCPKcl4 cells by activation of a PI-3 kinase–Akt-signaling pathway. (A) 14,15-EET's antiapoptotic effects were abolished by inhibition of PI-3 kinase but not by inhibition of MAP kinase. After pretreatment with or without the specific PI-3 kinase inhibitor wortmannin (10 nM) or LY294002 (5 μM) or the MEK inhibitor PD98059 (10 μM) for 30 min, followed by 14,15-EET or vehicle for 1 h, LLCPKcl4 cells were exposed to H2O2 for 24 h, and DNA laddering was assessed. (B) Arachidonic acid's antiapoptotic effects in BM3 cells were abolished by inhibition of PI-3 kinase but not by inhibition of MAP kinase. Before induction of H2O2-mediated apoptosis, BM3 cells were pretreated with or without wortmannin, LY294002, or PD98059 and then treated with or without arachidonic acid. (A and B) Leftmost lane, 100-bp DNA ladder; rightmost lane, lambda DNA-HindIII size marker. (C) 14,15-EET increased Akt kinase activity, which was abolished by either wortmannin or LY294002. After treatment with or without the specific PI-3 kinase inhibitor wortmannin (10 nM) or LY294002 (5 μM), LLCPKcl4 cells were treated with or without 14,15-EET. The cells were then lysed and subjected to immunoprecipitation and Akt kinase activity assay with histone H2B as a substrate.

Article Snippet: Leftmost lane, 100-bp DNA ladder; rightmost lane, lambda DNA- Hin dIII DNA size marker (Promega). (C) 14,15-EET decreased H 2 O 2 - or etoposide-induced apoptotic-cell number; cells were scored for morphological evidence of apoptosis as described in Materials and Methods.

Techniques: Activation Assay, Inhibition, DNA Laddering, Lambda DNA Preparation, Marker, Activity Assay, Immunoprecipitation, Kinase Assay

Antiapoptotic effects of exogenously administered 14,15-EET in LLCPKcl4 cells. (A) 14,15-EET prevented the renal epithelial cell line LLCPKcl4 from progressive loss of cell viability caused by serum deprivation. LLCPKcl4 cells grown to confluence were changed to serum-free medium. After 48 h, vehicle (Me2SO) or 14,15-EET (10 μM) was added every 3 days. After 10 days, the majority of the vehicle-treated cells had died while the 14,15-EET treated cells still maintained a confluent monolayer with normal morphology. (B) 14,15-EET inhibited DNA laddering induced by H2O2 or etoposide. After pretreatment with vehicle (Me2SO) or 14,15-EET (10 μM) for 1 h, quiescent LLCPKcl4 cells were exposed to H2O2 (500 μM) or etoposide (100 μM) for 24 h, and genomic DNA was extracted and electrophoresed on a 1.5% agarose gel containing ethidium bromide. Leftmost lane, 100-bp DNA ladder; rightmost lane, lambda DNA-HindIII DNA size marker (Promega). (C) 14,15-EET decreased H2O2- or etoposide-induced apoptotic-cell number; cells were scored for morphological evidence of apoptosis as described in Materials and Methods.

Journal:

Article Title: Cytochrome P450 Epoxygenase Metabolism of Arachidonic Acid Inhibits Apoptosis

doi: 10.1128/MCB.21.18.6322-6331.2001

Figure Lengend Snippet: Antiapoptotic effects of exogenously administered 14,15-EET in LLCPKcl4 cells. (A) 14,15-EET prevented the renal epithelial cell line LLCPKcl4 from progressive loss of cell viability caused by serum deprivation. LLCPKcl4 cells grown to confluence were changed to serum-free medium. After 48 h, vehicle (Me2SO) or 14,15-EET (10 μM) was added every 3 days. After 10 days, the majority of the vehicle-treated cells had died while the 14,15-EET treated cells still maintained a confluent monolayer with normal morphology. (B) 14,15-EET inhibited DNA laddering induced by H2O2 or etoposide. After pretreatment with vehicle (Me2SO) or 14,15-EET (10 μM) for 1 h, quiescent LLCPKcl4 cells were exposed to H2O2 (500 μM) or etoposide (100 μM) for 24 h, and genomic DNA was extracted and electrophoresed on a 1.5% agarose gel containing ethidium bromide. Leftmost lane, 100-bp DNA ladder; rightmost lane, lambda DNA-HindIII DNA size marker (Promega). (C) 14,15-EET decreased H2O2- or etoposide-induced apoptotic-cell number; cells were scored for morphological evidence of apoptosis as described in Materials and Methods.

Article Snippet: Leftmost lane, 100-bp DNA ladder; rightmost lane, lambda DNA- Hin dIII DNA size marker (Promega). (C) 14,15-EET decreased H 2 O 2 - or etoposide-induced apoptotic-cell number; cells were scored for morphological evidence of apoptosis as described in Materials and Methods.

Techniques: DNA Laddering, Agarose Gel Electrophoresis, Lambda DNA Preparation, Marker

Effects of endogenously produced 14,15-EET in LLCPKcl4 cells. Arachidonic acid blocked H2O2-induced apoptosis in BM3 cells but not in Vector cells. Quiescent BM3 cells and Vector cells were pretreated with or without arachidonic acid (10 μM) for 1 h before exposure to H2O2 for 24 h, and DNA laddering (A) and apoptotic cell number (B) were assessed as described in Materials and Methods. (A) Leftmost lane, 100-bp DNA ladder; rightmost lane, lambda DNA-HindIII DNA size marker.

Journal:

Article Title: Cytochrome P450 Epoxygenase Metabolism of Arachidonic Acid Inhibits Apoptosis

doi: 10.1128/MCB.21.18.6322-6331.2001

Figure Lengend Snippet: Effects of endogenously produced 14,15-EET in LLCPKcl4 cells. Arachidonic acid blocked H2O2-induced apoptosis in BM3 cells but not in Vector cells. Quiescent BM3 cells and Vector cells were pretreated with or without arachidonic acid (10 μM) for 1 h before exposure to H2O2 for 24 h, and DNA laddering (A) and apoptotic cell number (B) were assessed as described in Materials and Methods. (A) Leftmost lane, 100-bp DNA ladder; rightmost lane, lambda DNA-HindIII DNA size marker.

Article Snippet: Leftmost lane, 100-bp DNA ladder; rightmost lane, lambda DNA- Hin dIII DNA size marker (Promega). (C) 14,15-EET decreased H 2 O 2 - or etoposide-induced apoptotic-cell number; cells were scored for morphological evidence of apoptosis as described in Materials and Methods.

Techniques: Produced, Plasmid Preparation, DNA Laddering, Lambda DNA Preparation, Marker

Arachidonic acid induced apoptosis in Vector cells but not in BM3 cells. Quiescent BM3 cells and Vector cells were treated with or without arachidonic acid (10 μM) for 48 h in the absence of other apoptosis-inducing stimuli and then subjected to assessment of DNA laddering. Leftmost lane, 100-bp DNA ladder; rightmost lane, lambda DNA-HindIII size marker.

Journal:

Article Title: Cytochrome P450 Epoxygenase Metabolism of Arachidonic Acid Inhibits Apoptosis

doi: 10.1128/MCB.21.18.6322-6331.2001

Figure Lengend Snippet: Arachidonic acid induced apoptosis in Vector cells but not in BM3 cells. Quiescent BM3 cells and Vector cells were treated with or without arachidonic acid (10 μM) for 48 h in the absence of other apoptosis-inducing stimuli and then subjected to assessment of DNA laddering. Leftmost lane, 100-bp DNA ladder; rightmost lane, lambda DNA-HindIII size marker.

Article Snippet: Leftmost lane, 100-bp DNA ladder; rightmost lane, lambda DNA- Hin dIII DNA size marker (Promega). (C) 14,15-EET decreased H 2 O 2 - or etoposide-induced apoptotic-cell number; cells were scored for morphological evidence of apoptosis as described in Materials and Methods.

Techniques: Plasmid Preparation, DNA Laddering, Lambda DNA Preparation, Marker