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A loss of epidermal PLCdelta1 impairs epidermal barrier function through dysregulation of Ca2+ and p38 mitogen-activated protein kinase (MAPK) signaling. This study also reveals a possible link among PLCdelta1 downregulation, p38 MAPK hyperactivation, and barrier defects in psoriasis-like skin inflammation.
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PLCD1 acts as a tumour suppressor, by KIF3A-mediated suppression of ERK1/2/beta-catenin/MMP7 signalling, at least in part, in breast cancer.
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Nine of the 32 (28.1%) iCCA patients had gene mutations at chromosome 3p, totaling 11 mutations across five genes. Those included five (15.6%) BAP1 mutations, two each (6.3%) of CACNA2D3 and RASSF1 mutations, and one each (3.1%) of ATG7 and PLCD1 mutations. Six (18.8%) cases had concurrent loss of chromosome 3p and gene mutations.
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The PLCdelta1 negatively regulates autophagy, and PLCdelta1 suppression contributes to the tolerance of CRC cells harboring KRAS mutations to nutrient deprivation and anti-cancer drug treatment.
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Phospholipase C delta 1 is both a KLF15-regulated gene and a novel repressor of airway smooth muscle hypertrophy.
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High PLC delta expression is associated with breast cancer.
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slow phase of Gi/o-mediated TRPC4 activation was diminished by inhibiting RhoA or enhancing PLCdelta function
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Both unsaturated and saturated dioleoyl-phosphatidylinositol-(4,5)-bisphosphate successfully recruited PHPLCdelta1 to cell membranes.
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Neuropeptide Y decreased PLCD1 expression in HUVECs.
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PLC-delta1 and TRPV6 are critical actor of Ca(2+) homeostasis in CF human bronchial epithelial cells.
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Ectopic expression of PLCD1 inhibits breast tumor cell proliferation in vivo by inducing apoptosis and suppressed tumor cell migration by regulating cytoskeletal reorganization.
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PLCdelta1 is required for maintenance of homeostasis in skin and metabolic tissues. [review]
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Provide evidence for intramolecular interactions in the PLC-delta1 PH domain.
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Genotyping using microsatellite markers linked the families to the gene PLCD1 on chromosome 3p22.2. Sequence analysis of the gene detected one novel (p.Ser740ArgfsX19) and one previously reported mutation (p.Arg437X).
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A novel mutation in the PLCD1 gene, which leads to an aberrant splicing event, underlies autosomal recessive leuconychia.
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PLCD1 acts as a functional tumor suppressor and may serve as a biomarker for possible early detection and prognosis of chronic myeloid leukemia.
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Increased PLC-delta1 activity causes enhanced coronary vasomotility such as that seen in patients with coronary spastic angina.
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Mutations in this gene cause hereditary porcelain nails. Review.
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Significantly deregulated pathways in colorectal cancer were identified and repression of PLCD1 and PLCE1 expression, was validated.
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these data show that mutations in PLCD1 underlie hereditary leukonychia, revealing a gene involved in molecular control of nail growth.