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Amotl2a (show AMOTL2 ELISA Kits) function in the control of lateral line primordium cell proliferation is mediated together by the Hippo pathway effector Yap1 (show YAP1 ELISA Kits) and the Wnt (show WNT2 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) effector Lef1.
Lef1 has a role in regulating Dusp6 (show DUSP6 ELISA Kits) in formation of the zebrafish posterior lateral line primordium
Nlk2 (show NLK ELISA Kits) is essential for the phosphorylation and activation of Lef1 transcriptional activity in neural progenitor cells.
Lef1 is required for progenitor cell identity in the zebrafish lateral line primordium.
Lef1 sustains proliferation of leading zone progenitors, maintaining the primordium size and defining neuromast deposition rate.
Data conclude that lef1-mediated Wnt (show WNT2 ELISA Kits) signaling is involved in various aspects of primordium migration, although part of this implication is masked by a high level of developmental redundancy.
Data show cooperation between Dnmt3 and an H3K9 methyltransferase G9a (show EHMT2 ELISA Kits) in regulating lef1.
high-affinity binding sites for Tcf (show HNF4A ELISA Kits)/Lef1 within the boz promoter region
Canonical Wnt (show WNT2 ELISA Kits) signaling through Lef1 is required for hypothalamic neurogenesis.
Domain-specific regulation of foxP2 (show FOXP2 ELISA Kits) CNS expression by lef1.
leukemic stem cells are therefore more sensitive to loss of Tcf1 (show HNF1A ELISA Kits) and Lef1 than Hematopoietic Stem Cells in their self-renewal capacity.
Sp5/8 bind directly to GC boxes in Wnt (show WNT2 ELISA Kits) target gene enhancers and to adjacent, or distally positioned, chromatin-bound T-cell factor (Tcf) 1 (show HNF1A ELISA Kits)/lymphoid enhancer factor (Lef) 1 to facilitate recruitment of beta-catenin (show CTNNB1 ELISA Kits) to target gene enhancers.
This paper demonstrates a cell-intrinsic requirement for transcription factors TCF1 (show HNF1A ELISA Kits) and LEF1 for the development of all subsets of Natural Killer T cells.
this study gives new insights into transcriptional regulating mechanisms of Wnt (show WNT2 ELISA Kits)-mediated Isl1 (show ISL1 ELISA Kits) expression during cardiomyocyte differentiation.
data reveal LEF1 as a central regulator of iNKT cell number and Th2-type effector differentiation.
These findings provide evidence for the existance of a posititve feedback loop connecting survivin expression in tumor cells to PI3K/Akt enhanced beta-catenin-Tcf/Lef-dependent transcription followed by secretion of VEGF and angiogenesis.
TDG (show TDG ELISA Kits), as a new coactivator, promotes beta-catenin (show CTNNB1 ELISA Kits)/TCFs transactivation and functionally cooperates with CBP (show CREBBP ELISA Kits) in canonical Wnt (show WNT2 ELISA Kits) signaling.
TCF-1 (show HNF1A ELISA Kits) and LEF-1 adopted distinct genetic 'wiring' to promote the CD4 (show CD4 ELISA Kits)(+) T cell fate and establish CD8 (show CD8A ELISA Kits)(+) T cell identity.
Postnatal isoform switch and protein localization of LEF1 and TCF7L2 (show TCF7L2 ELISA Kits) transcription factors in cortical, thalamic, and mesencephalic regions of the adult mouse brain.
Activation of beta-catenin (show CTNNB1 ELISA Kits)/TCF (show HNF4A ELISA Kits) signaling by lysophosphatidic acid may be involved in neurogenesis by controlling the survival of neural precursors.
Tcf (show HNF4A ELISA Kits)/Lef genes encode factors of different activities, which function together in antagonistic or synergistic ways to modulate the intensity and outcome of Wnt (show WNT2 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) signalling and to trigger tissue-specific responses.
Interaction of Xom and LEF1/TCF (show HNF4A ELISA Kits)-factors is essential for ventral cell fate determination and LEF1/TCF (show HNF4A ELISA Kits) factors may function as a point of convergence to mediate the combined signaling of Wnt (show WNT2 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) and BMP4 (show BMP4 ELISA Kits)/Xom pathways during early embryogenesis.
The results suggest a role for beta-catenin (show CTNNB1 ELISA Kits)/LEF1-mediated transcription in both malignant transformation and metastasis of prostate cancer
The results describe a novel mutation in LEF1 causing dysregulation of Wnt/B catenin signaling in eyelid sebaceous cancinoma
LEF-1 and MITF (show MITF ELISA Kits) regulate tyrosinase (show TYR ELISA Kits) gene transcription in vitro via binding to its promoter.
Methylprednisolone can suppress Wnt (show WNT2 ELISA Kits) signaling pathway by down-regulating LEF-1 protein expression in chronic lymphocyte leukemia cells.
Overexpression of LEF1 is a favorable prognostic factor in childhood ALL.
Authors found that the N-terminus of delta-catenin (show CTNND2 ELISA Kits) bound to the middle region of LEF-1 unlike beta-catenin (show CTNNB1 ELISA Kits). Overexpressed delta-catenin (show CTNND2 ELISA Kits) entered the nucleus and inhibited LEF-1-mediated transcriptional activity in Bosc23 and DLD (show DLD ELISA Kits)-1 cell lines.
high LEF1 expression and mutation are associated with high-risk leukemia and our results also revealed that LEF1 high expression and/or gain-of-function mutations are involved in leukemogenesis of ALL.
Study found a negative correlation between miR (show MLXIP ELISA Kits)-34a and LEF1 expression in prostate cancer cell lines and tumors and that miR (show MLXIP ELISA Kits)-34a regulated epithelial-mesenchymal transition through direct binding to LEF1 mRNA 3' UTR (show UTS2R ELISA Kits) region and silencing its translation.
Our study suggests LEF1 expression in oral squamous cell carcinoma may play an important role in tumor progression and can be served as a predictor of poor prognosis for patients with oral squamous cell carcinoma.
Elevated TCF-1 (show HNF1A ELISA Kits) and LEF-1 expression is characteristic of malignant gliomas
The molecular characterisation of the porcine LEF1 gene and its association with number of teats and inverted teats in experimental and commercial populations, is described.
This gene encodes a transcription factor belonging to a family of proteins that share homology with the high mobility group protein-1. The protein encoded by this gene can bind to a functionally important site in the T-cell receptor-alpha enhancer, thereby conferring maximal enhancer activity. This transcription factor is involved in the Wnt signaling pathway, and it may function in hair cell differentiation and follicle morphogenesis. Mutations in this gene have been found in somatic sebaceous tumors. This gene has also been linked to other cancers, including androgen-independent prostate cancer. Alternative splicing results in multiple transcript variants.
lymphoid enhancer binding factor-1
, lymphoid enhancer-binding factor 1
, lymphoid enhancer-binding factor 1-like
, lymphoid enhancer binding factor 1 short isoform
, T cell-specific transcription factor 1-alpha
, lymphiod enhancer binding factor 1
, transcription factor LEF-1
, lymphoid enhancer binding factor 1