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ampk β1 polyclonal antibody  (Proteintech)


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    Proteintech ampk β1 polyclonal antibody
    Summary and working model of how CDX2-reinstatement selectively targets CRC stem cells (A) CRC stem cells, but not normal stem cells, are characterized by enhanced transcription of Wnt/β-catenin and YAP target genes that are established markers of CSCs. Both pathways are known to collaboratively enhance stemness in the colon. , (B) PF treatment activates <t>β1-specific</t> <t>AMPK,</t> reactivates a tumor suppressor pathway (SPS pathway; 1), which attempts to restore tight- (TJ) and adherens (AJ) junctions in the setting of bioenergetic stress. Bioenergetic stress (AMPK activation) and junction restoration reshapes two junction-informed stemness programs, leading to their catastrophic withdrawal: (i) the Hippo-YAP pathway is activated (2), resulting in YAP phosphorylation followed by proteasomal degradation, and consequently, its nuclear exclusion (3) and withdrawal of the YAP/TEAD transcriptional program; (ii) junctional sequestration of β-catenin and consequently, its nuclear exclusion (4) and termination of the β-catenin·TCF/LEF transcriptional program. CDX2 -reinstatement, and differentiation programs that accompanies the same, is likely via AMPK-dependent epigenetic events , (5). Once translated into protein, CDX2 is known to complete and displace β-catenin from TCF/LEF complexes (6), which further accentuates the impact of the SPS pathway on the β-catenin·TCF/LEF transcriptional program. (C) Schematic illustrates the cell state-specific impact of CDX2-reinstatement therapy and the impact of restoration of the stress polarity signaling (SPS) pathway. Pre- (top) and post- (bottom) treatment states of cancers (left) and healthy (right) epithelium are shown. Although activation of the SPS pathway enhances differentiation and junction formation in both cell states, the apoptotic fate is selectively seen in CDX2 -low CSCs.
    Ampk β1 Polyclonal Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ampk β1 polyclonal antibody/product/Proteintech
    Average 93 stars, based on 11 article reviews
    ampk β1 polyclonal antibody - by Bioz Stars, 2026-02
    93/100 stars

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    1) Product Images from "CANDiT: A machine learning framework for differentiation therapy in colorectal cancer"

    Article Title: CANDiT: A machine learning framework for differentiation therapy in colorectal cancer

    Journal: Cell Reports Medicine

    doi: 10.1016/j.xcrm.2025.102421

    Summary and working model of how CDX2-reinstatement selectively targets CRC stem cells (A) CRC stem cells, but not normal stem cells, are characterized by enhanced transcription of Wnt/β-catenin and YAP target genes that are established markers of CSCs. Both pathways are known to collaboratively enhance stemness in the colon. , (B) PF treatment activates β1-specific AMPK, reactivates a tumor suppressor pathway (SPS pathway; 1), which attempts to restore tight- (TJ) and adherens (AJ) junctions in the setting of bioenergetic stress. Bioenergetic stress (AMPK activation) and junction restoration reshapes two junction-informed stemness programs, leading to their catastrophic withdrawal: (i) the Hippo-YAP pathway is activated (2), resulting in YAP phosphorylation followed by proteasomal degradation, and consequently, its nuclear exclusion (3) and withdrawal of the YAP/TEAD transcriptional program; (ii) junctional sequestration of β-catenin and consequently, its nuclear exclusion (4) and termination of the β-catenin·TCF/LEF transcriptional program. CDX2 -reinstatement, and differentiation programs that accompanies the same, is likely via AMPK-dependent epigenetic events , (5). Once translated into protein, CDX2 is known to complete and displace β-catenin from TCF/LEF complexes (6), which further accentuates the impact of the SPS pathway on the β-catenin·TCF/LEF transcriptional program. (C) Schematic illustrates the cell state-specific impact of CDX2-reinstatement therapy and the impact of restoration of the stress polarity signaling (SPS) pathway. Pre- (top) and post- (bottom) treatment states of cancers (left) and healthy (right) epithelium are shown. Although activation of the SPS pathway enhances differentiation and junction formation in both cell states, the apoptotic fate is selectively seen in CDX2 -low CSCs.
    Figure Legend Snippet: Summary and working model of how CDX2-reinstatement selectively targets CRC stem cells (A) CRC stem cells, but not normal stem cells, are characterized by enhanced transcription of Wnt/β-catenin and YAP target genes that are established markers of CSCs. Both pathways are known to collaboratively enhance stemness in the colon. , (B) PF treatment activates β1-specific AMPK, reactivates a tumor suppressor pathway (SPS pathway; 1), which attempts to restore tight- (TJ) and adherens (AJ) junctions in the setting of bioenergetic stress. Bioenergetic stress (AMPK activation) and junction restoration reshapes two junction-informed stemness programs, leading to their catastrophic withdrawal: (i) the Hippo-YAP pathway is activated (2), resulting in YAP phosphorylation followed by proteasomal degradation, and consequently, its nuclear exclusion (3) and withdrawal of the YAP/TEAD transcriptional program; (ii) junctional sequestration of β-catenin and consequently, its nuclear exclusion (4) and termination of the β-catenin·TCF/LEF transcriptional program. CDX2 -reinstatement, and differentiation programs that accompanies the same, is likely via AMPK-dependent epigenetic events , (5). Once translated into protein, CDX2 is known to complete and displace β-catenin from TCF/LEF complexes (6), which further accentuates the impact of the SPS pathway on the β-catenin·TCF/LEF transcriptional program. (C) Schematic illustrates the cell state-specific impact of CDX2-reinstatement therapy and the impact of restoration of the stress polarity signaling (SPS) pathway. Pre- (top) and post- (bottom) treatment states of cancers (left) and healthy (right) epithelium are shown. Although activation of the SPS pathway enhances differentiation and junction formation in both cell states, the apoptotic fate is selectively seen in CDX2 -low CSCs.

    Techniques Used: Activation Assay, Phospho-proteomics



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    ampk β1 polyclonal antibody  (Proteintech)
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    Proteintech ampk β1 polyclonal antibody
    Summary and working model of how CDX2-reinstatement selectively targets CRC stem cells (A) CRC stem cells, but not normal stem cells, are characterized by enhanced transcription of Wnt/β-catenin and YAP target genes that are established markers of CSCs. Both pathways are known to collaboratively enhance stemness in the colon. , (B) PF treatment activates <t>β1-specific</t> <t>AMPK,</t> reactivates a tumor suppressor pathway (SPS pathway; 1), which attempts to restore tight- (TJ) and adherens (AJ) junctions in the setting of bioenergetic stress. Bioenergetic stress (AMPK activation) and junction restoration reshapes two junction-informed stemness programs, leading to their catastrophic withdrawal: (i) the Hippo-YAP pathway is activated (2), resulting in YAP phosphorylation followed by proteasomal degradation, and consequently, its nuclear exclusion (3) and withdrawal of the YAP/TEAD transcriptional program; (ii) junctional sequestration of β-catenin and consequently, its nuclear exclusion (4) and termination of the β-catenin·TCF/LEF transcriptional program. CDX2 -reinstatement, and differentiation programs that accompanies the same, is likely via AMPK-dependent epigenetic events , (5). Once translated into protein, CDX2 is known to complete and displace β-catenin from TCF/LEF complexes (6), which further accentuates the impact of the SPS pathway on the β-catenin·TCF/LEF transcriptional program. (C) Schematic illustrates the cell state-specific impact of CDX2-reinstatement therapy and the impact of restoration of the stress polarity signaling (SPS) pathway. Pre- (top) and post- (bottom) treatment states of cancers (left) and healthy (right) epithelium are shown. Although activation of the SPS pathway enhances differentiation and junction formation in both cell states, the apoptotic fate is selectively seen in CDX2 -low CSCs.
    Ampk β1 Polyclonal Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ampk β1 polyclonal antibody/product/Proteintech
    Average 93 stars, based on 1 article reviews
    ampk β1 polyclonal antibody - by Bioz Stars, 2026-02
    93/100 stars
    		  Buy from Supplier

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    Summary and working model of how CDX2-reinstatement selectively targets CRC stem cells (A) CRC stem cells, but not normal stem cells, are characterized by enhanced transcription of Wnt/β-catenin and YAP target genes that are established markers of CSCs. Both pathways are known to collaboratively enhance stemness in the colon. , (B) PF treatment activates β1-specific AMPK, reactivates a tumor suppressor pathway (SPS pathway; 1), which attempts to restore tight- (TJ) and adherens (AJ) junctions in the setting of bioenergetic stress. Bioenergetic stress (AMPK activation) and junction restoration reshapes two junction-informed stemness programs, leading to their catastrophic withdrawal: (i) the Hippo-YAP pathway is activated (2), resulting in YAP phosphorylation followed by proteasomal degradation, and consequently, its nuclear exclusion (3) and withdrawal of the YAP/TEAD transcriptional program; (ii) junctional sequestration of β-catenin and consequently, its nuclear exclusion (4) and termination of the β-catenin·TCF/LEF transcriptional program. CDX2 -reinstatement, and differentiation programs that accompanies the same, is likely via AMPK-dependent epigenetic events , (5). Once translated into protein, CDX2 is known to complete and displace β-catenin from TCF/LEF complexes (6), which further accentuates the impact of the SPS pathway on the β-catenin·TCF/LEF transcriptional program. (C) Schematic illustrates the cell state-specific impact of CDX2-reinstatement therapy and the impact of restoration of the stress polarity signaling (SPS) pathway. Pre- (top) and post- (bottom) treatment states of cancers (left) and healthy (right) epithelium are shown. Although activation of the SPS pathway enhances differentiation and junction formation in both cell states, the apoptotic fate is selectively seen in CDX2 -low CSCs.

    Journal: Cell Reports Medicine

    Article Title: CANDiT: A machine learning framework for differentiation therapy in colorectal cancer

    doi: 10.1016/j.xcrm.2025.102421

    Figure Lengend Snippet: Summary and working model of how CDX2-reinstatement selectively targets CRC stem cells (A) CRC stem cells, but not normal stem cells, are characterized by enhanced transcription of Wnt/β-catenin and YAP target genes that are established markers of CSCs. Both pathways are known to collaboratively enhance stemness in the colon. , (B) PF treatment activates β1-specific AMPK, reactivates a tumor suppressor pathway (SPS pathway; 1), which attempts to restore tight- (TJ) and adherens (AJ) junctions in the setting of bioenergetic stress. Bioenergetic stress (AMPK activation) and junction restoration reshapes two junction-informed stemness programs, leading to their catastrophic withdrawal: (i) the Hippo-YAP pathway is activated (2), resulting in YAP phosphorylation followed by proteasomal degradation, and consequently, its nuclear exclusion (3) and withdrawal of the YAP/TEAD transcriptional program; (ii) junctional sequestration of β-catenin and consequently, its nuclear exclusion (4) and termination of the β-catenin·TCF/LEF transcriptional program. CDX2 -reinstatement, and differentiation programs that accompanies the same, is likely via AMPK-dependent epigenetic events , (5). Once translated into protein, CDX2 is known to complete and displace β-catenin from TCF/LEF complexes (6), which further accentuates the impact of the SPS pathway on the β-catenin·TCF/LEF transcriptional program. (C) Schematic illustrates the cell state-specific impact of CDX2-reinstatement therapy and the impact of restoration of the stress polarity signaling (SPS) pathway. Pre- (top) and post- (bottom) treatment states of cancers (left) and healthy (right) epithelium are shown. Although activation of the SPS pathway enhances differentiation and junction formation in both cell states, the apoptotic fate is selectively seen in CDX2 -low CSCs.

    Article Snippet: AMPK β1 Polyclonal antibody , Proteintech , Cat#10308-1-AP, RRID: AB_513239.

    Techniques: Activation Assay, Phospho-proteomics