2012
DOI: 10.1128/mcb.05688-11
|View full text |Cite
|
Sign up to set email alerts
|

Prolyl Isomerase Pin1 Regulates Neuronal Differentiation via β-Catenin

Abstract: dThe Wnt/␤-catenin pathway promotes proliferation of neural progenitor cells (NPCs) at early stages and induces neuronal differentiation from NPCs at late stages, but the molecular mechanisms that control this stage-specific response are unclear. Pin1 is a prolyl isomerase that regulates cell signaling uniquely by controlling protein conformation after phosphorylation, but its role in neuronal differentiation is not known. Here we found that whereas Pin1 depletion suppresses neuronal differentiation, Pin1 over… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1

Citation Types

0
75
0

Year Published

2013
2013
2021
2021

Publication Types

Select...
8

Relationship

1
7

Authors

Journals

citations
Cited by 57 publications
(77 citation statements)
references
References 96 publications
(180 reference statements)
0
75
0
Order By: Relevance
“…The same effects were observed after silencing of Pin1 in cortical progenitor cells using lentiviral-mediated expression of a Pin1 short hairpin (sh) RNA reagent, but not when a control non-silencing shRNA was used (Figure 1g). Taken together with the demonstration that knockout of mouse Pin1 causes decreased neuronal differentiation in cultured cortical progenitor cells, 25 these results show that Pin1 promotes cortical neurogenesis. Moreover, they provide evidence that Gro/TLE1:Hes1 and Pin1 have opposite biological functions during cortical neuronal development.…”
Section: Resultsmentioning
confidence: 75%
See 1 more Smart Citation
“…The same effects were observed after silencing of Pin1 in cortical progenitor cells using lentiviral-mediated expression of a Pin1 short hairpin (sh) RNA reagent, but not when a control non-silencing shRNA was used (Figure 1g). Taken together with the demonstration that knockout of mouse Pin1 causes decreased neuronal differentiation in cultured cortical progenitor cells, 25 these results show that Pin1 promotes cortical neurogenesis. Moreover, they provide evidence that Gro/TLE1:Hes1 and Pin1 have opposite biological functions during cortical neuronal development.…”
Section: Resultsmentioning
confidence: 75%
“…Pharmacological inhibition, or shRNA-mediated silencing, of Pin1 activity in cortical progenitor cells causes decreased neuronal differentiation and increased numbers of cells expressing markers of the undifferentiated neural progenitor state, in agreement with recent studies showing that Pin1 knockout in mice decreases neuronal differentiation in cultured neural progenitor cells. 25 More importantly, we have shown that expression of Pin1 and HIPK2 blocks the ability of Gro/ TLE1:Hes1 to inhibit neuronal differentiation in both retinoic acid-treated SH-SY5Y neuroblastoma cells and primary cultures of cortical neural progenitor cells.…”
Section: Discussionmentioning
confidence: 97%
“…Pin1 also modulates several other signaling molecules involved in cell fate determination. By stabilizing ␤-catenin Pin1 induces neuronal differentiation of neural progenitor cells (16). A strong correlation between Pin1 expression and Notch activity has also been reported implicating Notch as a substrate mediating effects of Pin1 signaling and regulating proliferation and lineage commitment (17).…”
Section: Discussionmentioning
confidence: 99%
“…Lineage commitment and cell differentiation that are highly relevant in the context of stem cells are also dramatically influenced by Pin1. Pin1 maintains the balance between stem cell pluripotency, stemness, and commitment by stabilizing and activating molecules controlling self-renewal and differentiation (15)(16)(17). These provocative roles of Pin1 in the areas of proliferation, survival, senescence, and cell fate determination have tremendous impact on stem cell biology that remains unexplored in the context of CPCs.…”
mentioning
confidence: 99%
“…In vivo, Pin1 becomes highly expressed in nestin-positive neural progenitors between embryonic days E12.5 and E15.5 (37), precisely the time at which REST is down-regulated in cortical progenitors (3). Further, premature loss of Pin1 in mice, using nestin-driven Cre recombinase, results in fewer βIII tubulin positive neurons in the developing cerebral cortex (37). The authors proposed that Pin1 is required to stabilize β-catenin and thereby terminate expression of Wnt-activated proneural genes, such as neurogenin 1.…”
Section: Discussionmentioning
confidence: 99%