China 
Africa 
Explore chapters and articles related to this topic
Glaucoma
Published in Ching-Yu Cheng, Tien Yin Wong, Ophthalmic Epidemiology, 2022
Zhi Da Soh, Victor Koh, Ching-Yu Cheng
In addition, GWAS have identified several SNPs at different loci that are either associated directly with PACG itself, or through ocular features involved in its pathogenesis (e.g., anterior-chamber depth, trabecular meshwork, iris).124,172 These loci include, but are not limited to, PLEKHA7, COL11A1, PCMTD1, EPDR1, CHAT, GLIS3, FERMT2, and DRM2-FAM102.172,173 Taken together, these loci explain less than 2% of genetic variation in PACG,124 and exhibit little overlap between the genetic etiology of POAG and PACG.172
Breast Cancer
Published in Dongyou Liu, Tumors and Cancers, 2017
ILC often contains small, uniform, round cells in single file (linear, Indian file) or a targetoid pattern of noncohesive cells encircling ducts; evenly disbursed chromatin and no nucleoli (like LCIS cells); signet ring cells, intracellular lumina, and intracellular mucin; variable dense fibrous stroma with periductal and perivenous elastosis; dense lymphoid infiltrate; <10 mitoses/10 high-power field (HPF); and no necrosis. ILC is positive for ER, PR, HMW keratin, mucicarmine (intracellular mucin), GCDFP-15 (30%), and PLEKHA7, but negative for E-cadherin, p53, HER2, and Ki-67. Molecularly, ILC shows inactivation of E-cadherin, loss of heterozygosity, or methylation [6].
Interplay between EGFR, E-cadherin, and PTP1B in epidermal homeostasis
Published in Tissue Barriers, 2023
Tessa Arnaud, Fernando Rodrigues-Lima, Mireille Viguier, Frédérique Deshayes
Beyond the catenins, other partners of the AJ complex have been shown to be crucial in the interaction between EGFR and E-cadherin. PLEKHA7, a recently demonstrated new component of the AJ, is known to stabilize the molecular complex of E-cadherin by linking it to the minus ends of non-centrosomal microtubules.29 However, it also appears that this molecule obliterates the interaction between EGFR and E-cadherin since upon PLEKHA7 overexpression in epithelial ovarian cancer, the association of E-cadherin with EGFR is lost and subsequent EGFR activation inhibited.37,44 This type of interaction has also been illustrated for the neurofibromatosis type-2 (NF2) tumor suppressor and Merlin (also known as schwannomin). Merlin has been described to be recruited at the cadherin/catenin complex and to regulate cell adhesion.45,46 A few years later it has been demonstrated that it could also binds to and regulates EGFR trafficking through NHE-FR147 and hence by this interaction with both E-cadherin and EGFR coordinate membrane receptor signaling and adhesion in mammalian cells.48
The role of microtubules in the regulation of epithelial junctions
Published in Tissue Barriers, 2018
Ekaterina Vasileva, Sandra Citi
An important mechanism of MTs-AJ interaction was discovered with the identification of PLEKHA7, which binds to p120-ctn and to the minus-end MT-binding protein nezha/CAMSAP3, thus promoting the stabilization of the ZA through the accumulation of E-cadherin.61 In agreement, overexpression of PLEKHA7 attenuates, in a MT-dependent manner, the disruption of junctions and the increase in paracellular TJ-dependent permeability induced by depletion of extracellular calcium.97 PLEKHA7 binds to additional ZA proteins, such as paracingulin,74,98 afadin99 and PDZD11.100 PLEKHA7 is also involved in recruiting mRNAs and miRNA processing factors to the ZA, modulating cellular resistance to staphylococcal α-toxin and controlling the pathogenesis of hypertension and angle closure glaucoma, through mechanisms that remain to be clarified (reviewed in101). However, the role of MT-tethering in all these additional interactions and functions of PLEKHA7 is not clear.
Critical roles of adherens junctions in diseases of the oral mucosa
Published in Tissue Barriers, 2023
Christina Kingsley, Antonis Kourtidis
Furthermore, recent advances have revealed several new AJ components that are potentially involved in oral pathologies, such as PLEKHA7 and PLEKHA5 in NSCL/P.99 These proteins have been studied in other tissues and cells and have been shown to have important roles in AJ function and integrity.30,62,63,65,66,68,69,138 For example, PLEKHA7 has been shown to recruit and regulate the RNAi machinery at AJs.61,62 However, no mechanistic studies have been conducted on these AJ components with regard to the oral epithelium. Since dysregulation of AJs could impact miRNA function, and PLEKHA7 mutations have been correlated with NSCL/P, it would be interesting to examine whether this correlation is mechanistically explained through the miRNA-related or other reported functions of PLEKHA7. Ultimately, studies like these can pave the way for the development of novel therapeutics. For example, if AJ disruption leads to miRNA dysregulation, there is the potential use of RNAi as replacement therapy.139,140 Indeed, RNAi therapies in the context of cancers, such as oral cancer, could be an important new direction, as the limited current therapies have side effects. In addition, due to the important roles of β-catenin as a structural component of AJs and as a regulator in cancer progression during homeostasis, Wnt/β-catenin signaling could serve as another therapeutic target for HNSCC.141 Finally, recent work has revealed roles of ion channels, such as TRPV4, as being critical for the formation and stability of AJs in the junctional epithelium, and related their loss to periodontal disease, which could be another intriguing avenue of investigation.142,143