Bridging the gap between non-canonical and canonical Wnt signaling through Vangl2
Non-canonical Wnt signaling (encompassing Wnt/PCP and WntCa2+) has a dual identity in the literature. One stream of research investigates its role in antagonizing canonical Wnt/β-catenin signaling in cancer, typically through Ca2+, while the other stream investigates its effect on polarity in develo...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Bell, Ian James [verfasserIn] |
|---|
| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2022transfer abstract |
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| Schlagwörter: |
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| Umfang: |
8 |
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| Übergeordnetes Werk: |
Enthalten in: Spin-polarized bandgap of graphene induced by alternative chemisorption with MgO (111) substrate - Cho, Sung Beom ELSEVIER, 2014transfer abstract, London |
|---|---|
| Übergeordnetes Werk: |
volume:125 ; year:2022 ; pages:37-44 ; extent:8 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.semcdb.2021.10.004 |
|---|
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ELV057255350 |
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| 520 | |a Non-canonical Wnt signaling (encompassing Wnt/PCP and WntCa2+) has a dual identity in the literature. One stream of research investigates its role in antagonizing canonical Wnt/β-catenin signaling in cancer, typically through Ca2+, while the other stream investigates its effect on polarity in development, typically through Vangl2. Rarely do these topics intersect or overlap. What has become clear is that Wnt5a can mobilize intracellular calcium stores to inhibit Wnt/β-catenin in cancer cells but there is no evidence that Vangl2 is involved in this process. Conversely, Wnt5a can independently activate Vangl2 to affect polarity and migration but the role of calcium in this process is also limited. Further, Vangl2 has also been implicated in inhibiting Wnt/β-catenin signaling in development. The consensus is that a cell can differentiate between canonical and non-canonical Wnt signaling when presented with a choice, always choosing non-canonical at the expense of canonical Wnt signaling. However, these are rare events in vivo. Given the shared resources between non-canonical and canonical Wnt signaling it is perplexing that there is not more in vivo evidence for cross talk between these two pathways. In this review we discuss the intersection of non-canonical Wnt, with a focus on Wnt/PCP, and Wnt/β-catenin signaling in an attempt to shed some light on pathways that rarely meet at a crossroads in vivo. | ||
| 520 | |a Non-canonical Wnt signaling (encompassing Wnt/PCP and WntCa2+) has a dual identity in the literature. One stream of research investigates its role in antagonizing canonical Wnt/β-catenin signaling in cancer, typically through Ca2+, while the other stream investigates its effect on polarity in development, typically through Vangl2. Rarely do these topics intersect or overlap. What has become clear is that Wnt5a can mobilize intracellular calcium stores to inhibit Wnt/β-catenin in cancer cells but there is no evidence that Vangl2 is involved in this process. Conversely, Wnt5a can independently activate Vangl2 to affect polarity and migration but the role of calcium in this process is also limited. Further, Vangl2 has also been implicated in inhibiting Wnt/β-catenin signaling in development. The consensus is that a cell can differentiate between canonical and non-canonical Wnt signaling when presented with a choice, always choosing non-canonical at the expense of canonical Wnt signaling. However, these are rare events in vivo. Given the shared resources between non-canonical and canonical Wnt signaling it is perplexing that there is not more in vivo evidence for cross talk between these two pathways. In this review we discuss the intersection of non-canonical Wnt, with a focus on Wnt/PCP, and Wnt/β-catenin signaling in an attempt to shed some light on pathways that rarely meet at a crossroads in vivo. | ||
| 650 | 7 | |a Vangl2 |2 Elsevier | |
| 650 | 7 | |a Wnt/Calcium |2 Elsevier | |
| 650 | 7 | |a Wnt5a |2 Elsevier | |
| 650 | 7 | |a Wnt/β-catenin |2 Elsevier | |
| 650 | 7 | |a Wnt/PCP |2 Elsevier | |
| 650 | 7 | |a Wnt/Ca2+ |2 Elsevier | |
| 650 | 7 | |a Wnt |2 Elsevier | |
| 700 | 1 | |a Horn, Matthew Sheldon |4 oth | |
| 700 | 1 | |a Van Raay, Terence John |4 oth | |
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10.1016/j.semcdb.2021.10.004 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001720.pica (DE-627)ELV057255350 (ELSEVIER)S1084-9521(21)00267-6 DE-627 ger DE-627 rakwb eng 540 VZ 500 VZ 33.25 bkl 31.00 bkl Bell, Ian James verfasserin aut Bridging the gap between non-canonical and canonical Wnt signaling through Vangl2 2022transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Non-canonical Wnt signaling (encompassing Wnt/PCP and WntCa2+) has a dual identity in the literature. One stream of research investigates its role in antagonizing canonical Wnt/β-catenin signaling in cancer, typically through Ca2+, while the other stream investigates its effect on polarity in development, typically through Vangl2. Rarely do these topics intersect or overlap. What has become clear is that Wnt5a can mobilize intracellular calcium stores to inhibit Wnt/β-catenin in cancer cells but there is no evidence that Vangl2 is involved in this process. Conversely, Wnt5a can independently activate Vangl2 to affect polarity and migration but the role of calcium in this process is also limited. Further, Vangl2 has also been implicated in inhibiting Wnt/β-catenin signaling in development. The consensus is that a cell can differentiate between canonical and non-canonical Wnt signaling when presented with a choice, always choosing non-canonical at the expense of canonical Wnt signaling. However, these are rare events in vivo. Given the shared resources between non-canonical and canonical Wnt signaling it is perplexing that there is not more in vivo evidence for cross talk between these two pathways. In this review we discuss the intersection of non-canonical Wnt, with a focus on Wnt/PCP, and Wnt/β-catenin signaling in an attempt to shed some light on pathways that rarely meet at a crossroads in vivo. Non-canonical Wnt signaling (encompassing Wnt/PCP and WntCa2+) has a dual identity in the literature. One stream of research investigates its role in antagonizing canonical Wnt/β-catenin signaling in cancer, typically through Ca2+, while the other stream investigates its effect on polarity in development, typically through Vangl2. Rarely do these topics intersect or overlap. What has become clear is that Wnt5a can mobilize intracellular calcium stores to inhibit Wnt/β-catenin in cancer cells but there is no evidence that Vangl2 is involved in this process. Conversely, Wnt5a can independently activate Vangl2 to affect polarity and migration but the role of calcium in this process is also limited. Further, Vangl2 has also been implicated in inhibiting Wnt/β-catenin signaling in development. The consensus is that a cell can differentiate between canonical and non-canonical Wnt signaling when presented with a choice, always choosing non-canonical at the expense of canonical Wnt signaling. However, these are rare events in vivo. Given the shared resources between non-canonical and canonical Wnt signaling it is perplexing that there is not more in vivo evidence for cross talk between these two pathways. In this review we discuss the intersection of non-canonical Wnt, with a focus on Wnt/PCP, and Wnt/β-catenin signaling in an attempt to shed some light on pathways that rarely meet at a crossroads in vivo. Vangl2 Elsevier Wnt/Calcium Elsevier Wnt5a Elsevier Wnt/β-catenin Elsevier Wnt/PCP Elsevier Wnt/Ca2+ Elsevier Wnt Elsevier Horn, Matthew Sheldon oth Van Raay, Terence John oth Enthalten in Academic Press Cho, Sung Beom ELSEVIER Spin-polarized bandgap of graphene induced by alternative chemisorption with MgO (111) substrate 2014transfer abstract London (DE-627)ELV017968445 volume:125 year:2022 pages:37-44 extent:8 https://doi.org/10.1016/j.semcdb.2021.10.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-MAT GBV_ILN_70 33.25 Thermodynamik statistische Physik VZ 31.00 Mathematik: Allgemeines VZ AR 125 2022 37-44 8 |
| spelling |
10.1016/j.semcdb.2021.10.004 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001720.pica (DE-627)ELV057255350 (ELSEVIER)S1084-9521(21)00267-6 DE-627 ger DE-627 rakwb eng 540 VZ 500 VZ 33.25 bkl 31.00 bkl Bell, Ian James verfasserin aut Bridging the gap between non-canonical and canonical Wnt signaling through Vangl2 2022transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Non-canonical Wnt signaling (encompassing Wnt/PCP and WntCa2+) has a dual identity in the literature. One stream of research investigates its role in antagonizing canonical Wnt/β-catenin signaling in cancer, typically through Ca2+, while the other stream investigates its effect on polarity in development, typically through Vangl2. Rarely do these topics intersect or overlap. What has become clear is that Wnt5a can mobilize intracellular calcium stores to inhibit Wnt/β-catenin in cancer cells but there is no evidence that Vangl2 is involved in this process. Conversely, Wnt5a can independently activate Vangl2 to affect polarity and migration but the role of calcium in this process is also limited. Further, Vangl2 has also been implicated in inhibiting Wnt/β-catenin signaling in development. The consensus is that a cell can differentiate between canonical and non-canonical Wnt signaling when presented with a choice, always choosing non-canonical at the expense of canonical Wnt signaling. However, these are rare events in vivo. Given the shared resources between non-canonical and canonical Wnt signaling it is perplexing that there is not more in vivo evidence for cross talk between these two pathways. In this review we discuss the intersection of non-canonical Wnt, with a focus on Wnt/PCP, and Wnt/β-catenin signaling in an attempt to shed some light on pathways that rarely meet at a crossroads in vivo. Non-canonical Wnt signaling (encompassing Wnt/PCP and WntCa2+) has a dual identity in the literature. One stream of research investigates its role in antagonizing canonical Wnt/β-catenin signaling in cancer, typically through Ca2+, while the other stream investigates its effect on polarity in development, typically through Vangl2. Rarely do these topics intersect or overlap. What has become clear is that Wnt5a can mobilize intracellular calcium stores to inhibit Wnt/β-catenin in cancer cells but there is no evidence that Vangl2 is involved in this process. Conversely, Wnt5a can independently activate Vangl2 to affect polarity and migration but the role of calcium in this process is also limited. Further, Vangl2 has also been implicated in inhibiting Wnt/β-catenin signaling in development. The consensus is that a cell can differentiate between canonical and non-canonical Wnt signaling when presented with a choice, always choosing non-canonical at the expense of canonical Wnt signaling. However, these are rare events in vivo. Given the shared resources between non-canonical and canonical Wnt signaling it is perplexing that there is not more in vivo evidence for cross talk between these two pathways. In this review we discuss the intersection of non-canonical Wnt, with a focus on Wnt/PCP, and Wnt/β-catenin signaling in an attempt to shed some light on pathways that rarely meet at a crossroads in vivo. Vangl2 Elsevier Wnt/Calcium Elsevier Wnt5a Elsevier Wnt/β-catenin Elsevier Wnt/PCP Elsevier Wnt/Ca2+ Elsevier Wnt Elsevier Horn, Matthew Sheldon oth Van Raay, Terence John oth Enthalten in Academic Press Cho, Sung Beom ELSEVIER Spin-polarized bandgap of graphene induced by alternative chemisorption with MgO (111) substrate 2014transfer abstract London (DE-627)ELV017968445 volume:125 year:2022 pages:37-44 extent:8 https://doi.org/10.1016/j.semcdb.2021.10.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-MAT GBV_ILN_70 33.25 Thermodynamik statistische Physik VZ 31.00 Mathematik: Allgemeines VZ AR 125 2022 37-44 8 |
| allfields_unstemmed |
10.1016/j.semcdb.2021.10.004 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001720.pica (DE-627)ELV057255350 (ELSEVIER)S1084-9521(21)00267-6 DE-627 ger DE-627 rakwb eng 540 VZ 500 VZ 33.25 bkl 31.00 bkl Bell, Ian James verfasserin aut Bridging the gap between non-canonical and canonical Wnt signaling through Vangl2 2022transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Non-canonical Wnt signaling (encompassing Wnt/PCP and WntCa2+) has a dual identity in the literature. One stream of research investigates its role in antagonizing canonical Wnt/β-catenin signaling in cancer, typically through Ca2+, while the other stream investigates its effect on polarity in development, typically through Vangl2. Rarely do these topics intersect or overlap. What has become clear is that Wnt5a can mobilize intracellular calcium stores to inhibit Wnt/β-catenin in cancer cells but there is no evidence that Vangl2 is involved in this process. Conversely, Wnt5a can independently activate Vangl2 to affect polarity and migration but the role of calcium in this process is also limited. Further, Vangl2 has also been implicated in inhibiting Wnt/β-catenin signaling in development. The consensus is that a cell can differentiate between canonical and non-canonical Wnt signaling when presented with a choice, always choosing non-canonical at the expense of canonical Wnt signaling. However, these are rare events in vivo. Given the shared resources between non-canonical and canonical Wnt signaling it is perplexing that there is not more in vivo evidence for cross talk between these two pathways. In this review we discuss the intersection of non-canonical Wnt, with a focus on Wnt/PCP, and Wnt/β-catenin signaling in an attempt to shed some light on pathways that rarely meet at a crossroads in vivo. Non-canonical Wnt signaling (encompassing Wnt/PCP and WntCa2+) has a dual identity in the literature. One stream of research investigates its role in antagonizing canonical Wnt/β-catenin signaling in cancer, typically through Ca2+, while the other stream investigates its effect on polarity in development, typically through Vangl2. Rarely do these topics intersect or overlap. What has become clear is that Wnt5a can mobilize intracellular calcium stores to inhibit Wnt/β-catenin in cancer cells but there is no evidence that Vangl2 is involved in this process. Conversely, Wnt5a can independently activate Vangl2 to affect polarity and migration but the role of calcium in this process is also limited. Further, Vangl2 has also been implicated in inhibiting Wnt/β-catenin signaling in development. The consensus is that a cell can differentiate between canonical and non-canonical Wnt signaling when presented with a choice, always choosing non-canonical at the expense of canonical Wnt signaling. However, these are rare events in vivo. Given the shared resources between non-canonical and canonical Wnt signaling it is perplexing that there is not more in vivo evidence for cross talk between these two pathways. In this review we discuss the intersection of non-canonical Wnt, with a focus on Wnt/PCP, and Wnt/β-catenin signaling in an attempt to shed some light on pathways that rarely meet at a crossroads in vivo. Vangl2 Elsevier Wnt/Calcium Elsevier Wnt5a Elsevier Wnt/β-catenin Elsevier Wnt/PCP Elsevier Wnt/Ca2+ Elsevier Wnt Elsevier Horn, Matthew Sheldon oth Van Raay, Terence John oth Enthalten in Academic Press Cho, Sung Beom ELSEVIER Spin-polarized bandgap of graphene induced by alternative chemisorption with MgO (111) substrate 2014transfer abstract London (DE-627)ELV017968445 volume:125 year:2022 pages:37-44 extent:8 https://doi.org/10.1016/j.semcdb.2021.10.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-MAT GBV_ILN_70 33.25 Thermodynamik statistische Physik VZ 31.00 Mathematik: Allgemeines VZ AR 125 2022 37-44 8 |
| allfieldsGer |
10.1016/j.semcdb.2021.10.004 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001720.pica (DE-627)ELV057255350 (ELSEVIER)S1084-9521(21)00267-6 DE-627 ger DE-627 rakwb eng 540 VZ 500 VZ 33.25 bkl 31.00 bkl Bell, Ian James verfasserin aut Bridging the gap between non-canonical and canonical Wnt signaling through Vangl2 2022transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Non-canonical Wnt signaling (encompassing Wnt/PCP and WntCa2+) has a dual identity in the literature. One stream of research investigates its role in antagonizing canonical Wnt/β-catenin signaling in cancer, typically through Ca2+, while the other stream investigates its effect on polarity in development, typically through Vangl2. Rarely do these topics intersect or overlap. What has become clear is that Wnt5a can mobilize intracellular calcium stores to inhibit Wnt/β-catenin in cancer cells but there is no evidence that Vangl2 is involved in this process. Conversely, Wnt5a can independently activate Vangl2 to affect polarity and migration but the role of calcium in this process is also limited. Further, Vangl2 has also been implicated in inhibiting Wnt/β-catenin signaling in development. The consensus is that a cell can differentiate between canonical and non-canonical Wnt signaling when presented with a choice, always choosing non-canonical at the expense of canonical Wnt signaling. However, these are rare events in vivo. Given the shared resources between non-canonical and canonical Wnt signaling it is perplexing that there is not more in vivo evidence for cross talk between these two pathways. In this review we discuss the intersection of non-canonical Wnt, with a focus on Wnt/PCP, and Wnt/β-catenin signaling in an attempt to shed some light on pathways that rarely meet at a crossroads in vivo. Non-canonical Wnt signaling (encompassing Wnt/PCP and WntCa2+) has a dual identity in the literature. One stream of research investigates its role in antagonizing canonical Wnt/β-catenin signaling in cancer, typically through Ca2+, while the other stream investigates its effect on polarity in development, typically through Vangl2. Rarely do these topics intersect or overlap. What has become clear is that Wnt5a can mobilize intracellular calcium stores to inhibit Wnt/β-catenin in cancer cells but there is no evidence that Vangl2 is involved in this process. Conversely, Wnt5a can independently activate Vangl2 to affect polarity and migration but the role of calcium in this process is also limited. Further, Vangl2 has also been implicated in inhibiting Wnt/β-catenin signaling in development. The consensus is that a cell can differentiate between canonical and non-canonical Wnt signaling when presented with a choice, always choosing non-canonical at the expense of canonical Wnt signaling. However, these are rare events in vivo. Given the shared resources between non-canonical and canonical Wnt signaling it is perplexing that there is not more in vivo evidence for cross talk between these two pathways. In this review we discuss the intersection of non-canonical Wnt, with a focus on Wnt/PCP, and Wnt/β-catenin signaling in an attempt to shed some light on pathways that rarely meet at a crossroads in vivo. Vangl2 Elsevier Wnt/Calcium Elsevier Wnt5a Elsevier Wnt/β-catenin Elsevier Wnt/PCP Elsevier Wnt/Ca2+ Elsevier Wnt Elsevier Horn, Matthew Sheldon oth Van Raay, Terence John oth Enthalten in Academic Press Cho, Sung Beom ELSEVIER Spin-polarized bandgap of graphene induced by alternative chemisorption with MgO (111) substrate 2014transfer abstract London (DE-627)ELV017968445 volume:125 year:2022 pages:37-44 extent:8 https://doi.org/10.1016/j.semcdb.2021.10.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-MAT GBV_ILN_70 33.25 Thermodynamik statistische Physik VZ 31.00 Mathematik: Allgemeines VZ AR 125 2022 37-44 8 |
| allfieldsSound |
10.1016/j.semcdb.2021.10.004 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001720.pica (DE-627)ELV057255350 (ELSEVIER)S1084-9521(21)00267-6 DE-627 ger DE-627 rakwb eng 540 VZ 500 VZ 33.25 bkl 31.00 bkl Bell, Ian James verfasserin aut Bridging the gap between non-canonical and canonical Wnt signaling through Vangl2 2022transfer abstract 8 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Non-canonical Wnt signaling (encompassing Wnt/PCP and WntCa2+) has a dual identity in the literature. One stream of research investigates its role in antagonizing canonical Wnt/β-catenin signaling in cancer, typically through Ca2+, while the other stream investigates its effect on polarity in development, typically through Vangl2. Rarely do these topics intersect or overlap. What has become clear is that Wnt5a can mobilize intracellular calcium stores to inhibit Wnt/β-catenin in cancer cells but there is no evidence that Vangl2 is involved in this process. Conversely, Wnt5a can independently activate Vangl2 to affect polarity and migration but the role of calcium in this process is also limited. Further, Vangl2 has also been implicated in inhibiting Wnt/β-catenin signaling in development. The consensus is that a cell can differentiate between canonical and non-canonical Wnt signaling when presented with a choice, always choosing non-canonical at the expense of canonical Wnt signaling. However, these are rare events in vivo. Given the shared resources between non-canonical and canonical Wnt signaling it is perplexing that there is not more in vivo evidence for cross talk between these two pathways. In this review we discuss the intersection of non-canonical Wnt, with a focus on Wnt/PCP, and Wnt/β-catenin signaling in an attempt to shed some light on pathways that rarely meet at a crossroads in vivo. Non-canonical Wnt signaling (encompassing Wnt/PCP and WntCa2+) has a dual identity in the literature. One stream of research investigates its role in antagonizing canonical Wnt/β-catenin signaling in cancer, typically through Ca2+, while the other stream investigates its effect on polarity in development, typically through Vangl2. Rarely do these topics intersect or overlap. What has become clear is that Wnt5a can mobilize intracellular calcium stores to inhibit Wnt/β-catenin in cancer cells but there is no evidence that Vangl2 is involved in this process. Conversely, Wnt5a can independently activate Vangl2 to affect polarity and migration but the role of calcium in this process is also limited. Further, Vangl2 has also been implicated in inhibiting Wnt/β-catenin signaling in development. The consensus is that a cell can differentiate between canonical and non-canonical Wnt signaling when presented with a choice, always choosing non-canonical at the expense of canonical Wnt signaling. However, these are rare events in vivo. Given the shared resources between non-canonical and canonical Wnt signaling it is perplexing that there is not more in vivo evidence for cross talk between these two pathways. In this review we discuss the intersection of non-canonical Wnt, with a focus on Wnt/PCP, and Wnt/β-catenin signaling in an attempt to shed some light on pathways that rarely meet at a crossroads in vivo. Vangl2 Elsevier Wnt/Calcium Elsevier Wnt5a Elsevier Wnt/β-catenin Elsevier Wnt/PCP Elsevier Wnt/Ca2+ Elsevier Wnt Elsevier Horn, Matthew Sheldon oth Van Raay, Terence John oth Enthalten in Academic Press Cho, Sung Beom ELSEVIER Spin-polarized bandgap of graphene induced by alternative chemisorption with MgO (111) substrate 2014transfer abstract London (DE-627)ELV017968445 volume:125 year:2022 pages:37-44 extent:8 https://doi.org/10.1016/j.semcdb.2021.10.004 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-MAT GBV_ILN_70 33.25 Thermodynamik statistische Physik VZ 31.00 Mathematik: Allgemeines VZ AR 125 2022 37-44 8 |
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Enthalten in Spin-polarized bandgap of graphene induced by alternative chemisorption with MgO (111) substrate London volume:125 year:2022 pages:37-44 extent:8 |
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Bridging the gap between non-canonical and canonical Wnt signaling through Vangl2 |
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Non-canonical Wnt signaling (encompassing Wnt/PCP and WntCa2+) has a dual identity in the literature. One stream of research investigates its role in antagonizing canonical Wnt/β-catenin signaling in cancer, typically through Ca2+, while the other stream investigates its effect on polarity in development, typically through Vangl2. Rarely do these topics intersect or overlap. What has become clear is that Wnt5a can mobilize intracellular calcium stores to inhibit Wnt/β-catenin in cancer cells but there is no evidence that Vangl2 is involved in this process. Conversely, Wnt5a can independently activate Vangl2 to affect polarity and migration but the role of calcium in this process is also limited. Further, Vangl2 has also been implicated in inhibiting Wnt/β-catenin signaling in development. The consensus is that a cell can differentiate between canonical and non-canonical Wnt signaling when presented with a choice, always choosing non-canonical at the expense of canonical Wnt signaling. However, these are rare events in vivo. Given the shared resources between non-canonical and canonical Wnt signaling it is perplexing that there is not more in vivo evidence for cross talk between these two pathways. In this review we discuss the intersection of non-canonical Wnt, with a focus on Wnt/PCP, and Wnt/β-catenin signaling in an attempt to shed some light on pathways that rarely meet at a crossroads in vivo. |
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Non-canonical Wnt signaling (encompassing Wnt/PCP and WntCa2+) has a dual identity in the literature. One stream of research investigates its role in antagonizing canonical Wnt/β-catenin signaling in cancer, typically through Ca2+, while the other stream investigates its effect on polarity in development, typically through Vangl2. Rarely do these topics intersect or overlap. What has become clear is that Wnt5a can mobilize intracellular calcium stores to inhibit Wnt/β-catenin in cancer cells but there is no evidence that Vangl2 is involved in this process. Conversely, Wnt5a can independently activate Vangl2 to affect polarity and migration but the role of calcium in this process is also limited. Further, Vangl2 has also been implicated in inhibiting Wnt/β-catenin signaling in development. The consensus is that a cell can differentiate between canonical and non-canonical Wnt signaling when presented with a choice, always choosing non-canonical at the expense of canonical Wnt signaling. However, these are rare events in vivo. Given the shared resources between non-canonical and canonical Wnt signaling it is perplexing that there is not more in vivo evidence for cross talk between these two pathways. In this review we discuss the intersection of non-canonical Wnt, with a focus on Wnt/PCP, and Wnt/β-catenin signaling in an attempt to shed some light on pathways that rarely meet at a crossroads in vivo. |
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Non-canonical Wnt signaling (encompassing Wnt/PCP and WntCa2+) has a dual identity in the literature. One stream of research investigates its role in antagonizing canonical Wnt/β-catenin signaling in cancer, typically through Ca2+, while the other stream investigates its effect on polarity in development, typically through Vangl2. Rarely do these topics intersect or overlap. What has become clear is that Wnt5a can mobilize intracellular calcium stores to inhibit Wnt/β-catenin in cancer cells but there is no evidence that Vangl2 is involved in this process. Conversely, Wnt5a can independently activate Vangl2 to affect polarity and migration but the role of calcium in this process is also limited. Further, Vangl2 has also been implicated in inhibiting Wnt/β-catenin signaling in development. The consensus is that a cell can differentiate between canonical and non-canonical Wnt signaling when presented with a choice, always choosing non-canonical at the expense of canonical Wnt signaling. However, these are rare events in vivo. Given the shared resources between non-canonical and canonical Wnt signaling it is perplexing that there is not more in vivo evidence for cross talk between these two pathways. In this review we discuss the intersection of non-canonical Wnt, with a focus on Wnt/PCP, and Wnt/β-catenin signaling in an attempt to shed some light on pathways that rarely meet at a crossroads in vivo. |
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