phosphorylation defective creb m1 Search Results


m-1  (ATCC)
98
ATCC m-1
M 1, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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gene exp atf4 mm00515324 m1  (Thermo Fisher)
99
Thermo Fisher gene exp atf4 mm00515324 m1
Schematic of the UPR cycle. The UPR encompasses at least three pathways that are activated by the accumulation of unfolded or misfolded proteins. The PERK pathway is one of these and is activated by phosphorylation of the eIF2α protein to suppress global protein synthesis while activating expression of a series of transcription factors, including <t>ATF4</t> and CHOP. CHOP expression is an important marker of PERK pathway activation, but our data suggest that it is unlikely to be a rate-limiting step. Nonetheless, CHOP expression is an obligatory step, which induces GADD34 expression, leading to dephosphorylation of phospho-eIF2α and the resumption of global protein synthesis. At this point of rekindled ribosome assembly, stochastic processes, such as the loss of calcium from endoplasmic reticulum stores, ATP depletion, redox changes/oxidative stress, or increased metabolism mediated by extrinsic growth factor signaling through cell surface receptors, may render cells transiently vulnerable to cell death as they attempt to restore normal cell function, leading to context-dependent and cell type-specific demise. In the event that cells reestablish homeostasis, subsequent metabolic events, such as the expression of a mutant protein in the case of rsh mice, cause protein aggregation and drive another UPR cycle and another period of stochastic vulnerability as the cell emerges from the UPR. Such periodic entry and exit from successive UPR cycles may continue for days or weeks or until the cell succumbs to apoptosis. Further, the more rapid or severe the accumulation of mutant proteins, the more frequently the cell activates the UPR and the greater the cumulative risk for apoptosis.
Gene Exp Atf4 Mm00515324 M1, supplied by Thermo Fisher, 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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phosphorylation defective creb m1  (Addgene inc)
93
Addgene inc phosphorylation defective creb m1
Schematic of the UPR cycle. The UPR encompasses at least three pathways that are activated by the accumulation of unfolded or misfolded proteins. The PERK pathway is one of these and is activated by phosphorylation of the eIF2α protein to suppress global protein synthesis while activating expression of a series of transcription factors, including <t>ATF4</t> and CHOP. CHOP expression is an important marker of PERK pathway activation, but our data suggest that it is unlikely to be a rate-limiting step. Nonetheless, CHOP expression is an obligatory step, which induces GADD34 expression, leading to dephosphorylation of phospho-eIF2α and the resumption of global protein synthesis. At this point of rekindled ribosome assembly, stochastic processes, such as the loss of calcium from endoplasmic reticulum stores, ATP depletion, redox changes/oxidative stress, or increased metabolism mediated by extrinsic growth factor signaling through cell surface receptors, may render cells transiently vulnerable to cell death as they attempt to restore normal cell function, leading to context-dependent and cell type-specific demise. In the event that cells reestablish homeostasis, subsequent metabolic events, such as the expression of a mutant protein in the case of rsh mice, cause protein aggregation and drive another UPR cycle and another period of stochastic vulnerability as the cell emerges from the UPR. Such periodic entry and exit from successive UPR cycles may continue for days or weeks or until the cell succumbs to apoptosis. Further, the more rapid or severe the accumulation of mutant proteins, the more frequently the cell activates the UPR and the greater the cumulative risk for apoptosis.
Phosphorylation Defective Creb M1, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mva-np+m1  (Vaccitech Ltd)
90
Vaccitech Ltd mva-np+m1
Schematic of the UPR cycle. The UPR encompasses at least three pathways that are activated by the accumulation of unfolded or misfolded proteins. The PERK pathway is one of these and is activated by phosphorylation of the eIF2α protein to suppress global protein synthesis while activating expression of a series of transcription factors, including <t>ATF4</t> and CHOP. CHOP expression is an important marker of PERK pathway activation, but our data suggest that it is unlikely to be a rate-limiting step. Nonetheless, CHOP expression is an obligatory step, which induces GADD34 expression, leading to dephosphorylation of phospho-eIF2α and the resumption of global protein synthesis. At this point of rekindled ribosome assembly, stochastic processes, such as the loss of calcium from endoplasmic reticulum stores, ATP depletion, redox changes/oxidative stress, or increased metabolism mediated by extrinsic growth factor signaling through cell surface receptors, may render cells transiently vulnerable to cell death as they attempt to restore normal cell function, leading to context-dependent and cell type-specific demise. In the event that cells reestablish homeostasis, subsequent metabolic events, such as the expression of a mutant protein in the case of rsh mice, cause protein aggregation and drive another UPR cycle and another period of stochastic vulnerability as the cell emerges from the UPR. Such periodic entry and exit from successive UPR cycles may continue for days or weeks or until the cell succumbs to apoptosis. Further, the more rapid or severe the accumulation of mutant proteins, the more frequently the cell activates the UPR and the greater the cumulative risk for apoptosis.
Mva Np+M1, supplied by Vaccitech Ltd, 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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digital camera dx m 1 200  (Nikon)
96
Nikon digital camera dx m 1 200
Schematic of the UPR cycle. The UPR encompasses at least three pathways that are activated by the accumulation of unfolded or misfolded proteins. The PERK pathway is one of these and is activated by phosphorylation of the eIF2α protein to suppress global protein synthesis while activating expression of a series of transcription factors, including <t>ATF4</t> and CHOP. CHOP expression is an important marker of PERK pathway activation, but our data suggest that it is unlikely to be a rate-limiting step. Nonetheless, CHOP expression is an obligatory step, which induces GADD34 expression, leading to dephosphorylation of phospho-eIF2α and the resumption of global protein synthesis. At this point of rekindled ribosome assembly, stochastic processes, such as the loss of calcium from endoplasmic reticulum stores, ATP depletion, redox changes/oxidative stress, or increased metabolism mediated by extrinsic growth factor signaling through cell surface receptors, may render cells transiently vulnerable to cell death as they attempt to restore normal cell function, leading to context-dependent and cell type-specific demise. In the event that cells reestablish homeostasis, subsequent metabolic events, such as the expression of a mutant protein in the case of rsh mice, cause protein aggregation and drive another UPR cycle and another period of stochastic vulnerability as the cell emerges from the UPR. Such periodic entry and exit from successive UPR cycles may continue for days or weeks or until the cell succumbs to apoptosis. Further, the more rapid or severe the accumulation of mutant proteins, the more frequently the cell activates the UPR and the greater the cumulative risk for apoptosis.
Digital Camera Dx M 1 200, supplied by Nikon, 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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aflatoxin m 1 (afm 1)  (Fermentek Ltd)
90
Fermentek Ltd aflatoxin m 1 (afm 1)
Schematic of the UPR cycle. The UPR encompasses at least three pathways that are activated by the accumulation of unfolded or misfolded proteins. The PERK pathway is one of these and is activated by phosphorylation of the eIF2α protein to suppress global protein synthesis while activating expression of a series of transcription factors, including <t>ATF4</t> and CHOP. CHOP expression is an important marker of PERK pathway activation, but our data suggest that it is unlikely to be a rate-limiting step. Nonetheless, CHOP expression is an obligatory step, which induces GADD34 expression, leading to dephosphorylation of phospho-eIF2α and the resumption of global protein synthesis. At this point of rekindled ribosome assembly, stochastic processes, such as the loss of calcium from endoplasmic reticulum stores, ATP depletion, redox changes/oxidative stress, or increased metabolism mediated by extrinsic growth factor signaling through cell surface receptors, may render cells transiently vulnerable to cell death as they attempt to restore normal cell function, leading to context-dependent and cell type-specific demise. In the event that cells reestablish homeostasis, subsequent metabolic events, such as the expression of a mutant protein in the case of rsh mice, cause protein aggregation and drive another UPR cycle and another period of stochastic vulnerability as the cell emerges from the UPR. Such periodic entry and exit from successive UPR cycles may continue for days or weeks or until the cell succumbs to apoptosis. Further, the more rapid or severe the accumulation of mutant proteins, the more frequently the cell activates the UPR and the greater the cumulative risk for apoptosis.
Aflatoxin M 1 (Afm 1), supplied by Fermentek Ltd, 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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lnt l  (World Precision Instruments)
93
World Precision Instruments lnt l
Schematic of the UPR cycle. The UPR encompasses at least three pathways that are activated by the accumulation of unfolded or misfolded proteins. The PERK pathway is one of these and is activated by phosphorylation of the eIF2α protein to suppress global protein synthesis while activating expression of a series of transcription factors, including <t>ATF4</t> and CHOP. CHOP expression is an important marker of PERK pathway activation, but our data suggest that it is unlikely to be a rate-limiting step. Nonetheless, CHOP expression is an obligatory step, which induces GADD34 expression, leading to dephosphorylation of phospho-eIF2α and the resumption of global protein synthesis. At this point of rekindled ribosome assembly, stochastic processes, such as the loss of calcium from endoplasmic reticulum stores, ATP depletion, redox changes/oxidative stress, or increased metabolism mediated by extrinsic growth factor signaling through cell surface receptors, may render cells transiently vulnerable to cell death as they attempt to restore normal cell function, leading to context-dependent and cell type-specific demise. In the event that cells reestablish homeostasis, subsequent metabolic events, such as the expression of a mutant protein in the case of rsh mice, cause protein aggregation and drive another UPR cycle and another period of stochastic vulnerability as the cell emerges from the UPR. Such periodic entry and exit from successive UPR cycles may continue for days or weeks or until the cell succumbs to apoptosis. Further, the more rapid or severe the accumulation of mutant proteins, the more frequently the cell activates the UPR and the greater the cumulative risk for apoptosis.
Lnt L, supplied by World Precision Instruments, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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lnt l - by Bioz Stars, 2026-02
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aflatoxin m 1 (afm 1  (Romer Labs Inc)
90
Romer Labs Inc aflatoxin m 1 (afm 1
Schematic of the UPR cycle. The UPR encompasses at least three pathways that are activated by the accumulation of unfolded or misfolded proteins. The PERK pathway is one of these and is activated by phosphorylation of the eIF2α protein to suppress global protein synthesis while activating expression of a series of transcription factors, including <t>ATF4</t> and CHOP. CHOP expression is an important marker of PERK pathway activation, but our data suggest that it is unlikely to be a rate-limiting step. Nonetheless, CHOP expression is an obligatory step, which induces GADD34 expression, leading to dephosphorylation of phospho-eIF2α and the resumption of global protein synthesis. At this point of rekindled ribosome assembly, stochastic processes, such as the loss of calcium from endoplasmic reticulum stores, ATP depletion, redox changes/oxidative stress, or increased metabolism mediated by extrinsic growth factor signaling through cell surface receptors, may render cells transiently vulnerable to cell death as they attempt to restore normal cell function, leading to context-dependent and cell type-specific demise. In the event that cells reestablish homeostasis, subsequent metabolic events, such as the expression of a mutant protein in the case of rsh mice, cause protein aggregation and drive another UPR cycle and another period of stochastic vulnerability as the cell emerges from the UPR. Such periodic entry and exit from successive UPR cycles may continue for days or weeks or until the cell succumbs to apoptosis. Further, the more rapid or severe the accumulation of mutant proteins, the more frequently the cell activates the UPR and the greater the cumulative risk for apoptosis.
Aflatoxin M 1 (Afm 1, supplied by Romer Labs Inc, 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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aflatoxin m 1 (afm 1  (Millipore)
90
Millipore aflatoxin m 1 (afm 1
Schematic of the UPR cycle. The UPR encompasses at least three pathways that are activated by the accumulation of unfolded or misfolded proteins. The PERK pathway is one of these and is activated by phosphorylation of the eIF2α protein to suppress global protein synthesis while activating expression of a series of transcription factors, including <t>ATF4</t> and CHOP. CHOP expression is an important marker of PERK pathway activation, but our data suggest that it is unlikely to be a rate-limiting step. Nonetheless, CHOP expression is an obligatory step, which induces GADD34 expression, leading to dephosphorylation of phospho-eIF2α and the resumption of global protein synthesis. At this point of rekindled ribosome assembly, stochastic processes, such as the loss of calcium from endoplasmic reticulum stores, ATP depletion, redox changes/oxidative stress, or increased metabolism mediated by extrinsic growth factor signaling through cell surface receptors, may render cells transiently vulnerable to cell death as they attempt to restore normal cell function, leading to context-dependent and cell type-specific demise. In the event that cells reestablish homeostasis, subsequent metabolic events, such as the expression of a mutant protein in the case of rsh mice, cause protein aggregation and drive another UPR cycle and another period of stochastic vulnerability as the cell emerges from the UPR. Such periodic entry and exit from successive UPR cycles may continue for days or weeks or until the cell succumbs to apoptosis. Further, the more rapid or severe the accumulation of mutant proteins, the more frequently the cell activates the UPR and the greater the cumulative risk for apoptosis.
Aflatoxin M 1 (Afm 1, 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
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ridascreen aflatoxin m 1  (R-Biopharm)
90
R-Biopharm ridascreen aflatoxin m 1
Schematic of the UPR cycle. The UPR encompasses at least three pathways that are activated by the accumulation of unfolded or misfolded proteins. The PERK pathway is one of these and is activated by phosphorylation of the eIF2α protein to suppress global protein synthesis while activating expression of a series of transcription factors, including <t>ATF4</t> and CHOP. CHOP expression is an important marker of PERK pathway activation, but our data suggest that it is unlikely to be a rate-limiting step. Nonetheless, CHOP expression is an obligatory step, which induces GADD34 expression, leading to dephosphorylation of phospho-eIF2α and the resumption of global protein synthesis. At this point of rekindled ribosome assembly, stochastic processes, such as the loss of calcium from endoplasmic reticulum stores, ATP depletion, redox changes/oxidative stress, or increased metabolism mediated by extrinsic growth factor signaling through cell surface receptors, may render cells transiently vulnerable to cell death as they attempt to restore normal cell function, leading to context-dependent and cell type-specific demise. In the event that cells reestablish homeostasis, subsequent metabolic events, such as the expression of a mutant protein in the case of rsh mice, cause protein aggregation and drive another UPR cycle and another period of stochastic vulnerability as the cell emerges from the UPR. Such periodic entry and exit from successive UPR cycles may continue for days or weeks or until the cell succumbs to apoptosis. Further, the more rapid or severe the accumulation of mutant proteins, the more frequently the cell activates the UPR and the greater the cumulative risk for apoptosis.
Ridascreen Aflatoxin M 1, supplied by R-Biopharm, 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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aflatoxin m 1 (afm 1)  (Biopure Corporation)
90
Biopure Corporation aflatoxin m 1 (afm 1)
Schematic of the UPR cycle. The UPR encompasses at least three pathways that are activated by the accumulation of unfolded or misfolded proteins. The PERK pathway is one of these and is activated by phosphorylation of the eIF2α protein to suppress global protein synthesis while activating expression of a series of transcription factors, including <t>ATF4</t> and CHOP. CHOP expression is an important marker of PERK pathway activation, but our data suggest that it is unlikely to be a rate-limiting step. Nonetheless, CHOP expression is an obligatory step, which induces GADD34 expression, leading to dephosphorylation of phospho-eIF2α and the resumption of global protein synthesis. At this point of rekindled ribosome assembly, stochastic processes, such as the loss of calcium from endoplasmic reticulum stores, ATP depletion, redox changes/oxidative stress, or increased metabolism mediated by extrinsic growth factor signaling through cell surface receptors, may render cells transiently vulnerable to cell death as they attempt to restore normal cell function, leading to context-dependent and cell type-specific demise. In the event that cells reestablish homeostasis, subsequent metabolic events, such as the expression of a mutant protein in the case of rsh mice, cause protein aggregation and drive another UPR cycle and another period of stochastic vulnerability as the cell emerges from the UPR. Such periodic entry and exit from successive UPR cycles may continue for days or weeks or until the cell succumbs to apoptosis. Further, the more rapid or severe the accumulation of mutant proteins, the more frequently the cell activates the UPR and the greater the cumulative risk for apoptosis.
Aflatoxin M 1 (Afm 1), supplied by Biopure Corporation, 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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aflatoxin m 1  (Millipore)
90
Millipore aflatoxin m 1
Schematic of the UPR cycle. The UPR encompasses at least three pathways that are activated by the accumulation of unfolded or misfolded proteins. The PERK pathway is one of these and is activated by phosphorylation of the eIF2α protein to suppress global protein synthesis while activating expression of a series of transcription factors, including <t>ATF4</t> and CHOP. CHOP expression is an important marker of PERK pathway activation, but our data suggest that it is unlikely to be a rate-limiting step. Nonetheless, CHOP expression is an obligatory step, which induces GADD34 expression, leading to dephosphorylation of phospho-eIF2α and the resumption of global protein synthesis. At this point of rekindled ribosome assembly, stochastic processes, such as the loss of calcium from endoplasmic reticulum stores, ATP depletion, redox changes/oxidative stress, or increased metabolism mediated by extrinsic growth factor signaling through cell surface receptors, may render cells transiently vulnerable to cell death as they attempt to restore normal cell function, leading to context-dependent and cell type-specific demise. In the event that cells reestablish homeostasis, subsequent metabolic events, such as the expression of a mutant protein in the case of rsh mice, cause protein aggregation and drive another UPR cycle and another period of stochastic vulnerability as the cell emerges from the UPR. Such periodic entry and exit from successive UPR cycles may continue for days or weeks or until the cell succumbs to apoptosis. Further, the more rapid or severe the accumulation of mutant proteins, the more frequently the cell activates the UPR and the greater the cumulative risk for apoptosis.
Aflatoxin M 1, 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
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aflatoxin m 1 - by Bioz Stars, 2026-02
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Schematic of the UPR cycle. The UPR encompasses at least three pathways that are activated by the accumulation of unfolded or misfolded proteins. The PERK pathway is one of these and is activated by phosphorylation of the eIF2α protein to suppress global protein synthesis while activating expression of a series of transcription factors, including ATF4 and CHOP. CHOP expression is an important marker of PERK pathway activation, but our data suggest that it is unlikely to be a rate-limiting step. Nonetheless, CHOP expression is an obligatory step, which induces GADD34 expression, leading to dephosphorylation of phospho-eIF2α and the resumption of global protein synthesis. At this point of rekindled ribosome assembly, stochastic processes, such as the loss of calcium from endoplasmic reticulum stores, ATP depletion, redox changes/oxidative stress, or increased metabolism mediated by extrinsic growth factor signaling through cell surface receptors, may render cells transiently vulnerable to cell death as they attempt to restore normal cell function, leading to context-dependent and cell type-specific demise. In the event that cells reestablish homeostasis, subsequent metabolic events, such as the expression of a mutant protein in the case of rsh mice, cause protein aggregation and drive another UPR cycle and another period of stochastic vulnerability as the cell emerges from the UPR. Such periodic entry and exit from successive UPR cycles may continue for days or weeks or until the cell succumbs to apoptosis. Further, the more rapid or severe the accumulation of mutant proteins, the more frequently the cell activates the UPR and the greater the cumulative risk for apoptosis.

Journal: The Journal of Neuroscience

Article Title: Overexpression of CHOP in Myelinating Cells Does Not Confer a Significant Phenotype under Normal or Metabolic Stress Conditions

doi: 10.1523/JNEUROSCI.1118-15.2016

Figure Lengend Snippet: Schematic of the UPR cycle. The UPR encompasses at least three pathways that are activated by the accumulation of unfolded or misfolded proteins. The PERK pathway is one of these and is activated by phosphorylation of the eIF2α protein to suppress global protein synthesis while activating expression of a series of transcription factors, including ATF4 and CHOP. CHOP expression is an important marker of PERK pathway activation, but our data suggest that it is unlikely to be a rate-limiting step. Nonetheless, CHOP expression is an obligatory step, which induces GADD34 expression, leading to dephosphorylation of phospho-eIF2α and the resumption of global protein synthesis. At this point of rekindled ribosome assembly, stochastic processes, such as the loss of calcium from endoplasmic reticulum stores, ATP depletion, redox changes/oxidative stress, or increased metabolism mediated by extrinsic growth factor signaling through cell surface receptors, may render cells transiently vulnerable to cell death as they attempt to restore normal cell function, leading to context-dependent and cell type-specific demise. In the event that cells reestablish homeostasis, subsequent metabolic events, such as the expression of a mutant protein in the case of rsh mice, cause protein aggregation and drive another UPR cycle and another period of stochastic vulnerability as the cell emerges from the UPR. Such periodic entry and exit from successive UPR cycles may continue for days or weeks or until the cell succumbs to apoptosis. Further, the more rapid or severe the accumulation of mutant proteins, the more frequently the cell activates the UPR and the greater the cumulative risk for apoptosis.

Article Snippet: Details of mouse-specific TaqMan probes (Invitrogen) used in this study were as follows: Atf3 , Mm00476032_m1; Atf4 , Mm00515324_m1; Atf6 , Mm01295319_m1; Bak, Mm00432045_m1; Bax , Mm00432051_m1; Bim , Mm00437796_m1; Bip , Mm00517691_m1; Caspase3 , Mm01195085_m1; Chop , endogenous ( Chop i ), Mm00492097_m1; Chop , total (endogenous + transgene), Mm01135937_g1; Der2 , Mm00504288_m1; Gadd34 , Mm00435119_m1*; Herpdu , Mm00445600_m1; Mbp , Mm01262037_m1; Mog , Mm00447824_m1; p21 CIP , Mm04207341_m1; Plp1 , Mm01297210_m1; Xbp1 splice , Mm00457357_m1*; and Tbp , Mm00446973_m1.

Techniques: Phospho-proteomics, Expressing, Marker, Activation Assay, De-Phosphorylation Assay, Cell Function Assay, Mutagenesis