Disease relevance of PRICKLE1

• Prickle-1 Negatively Regulates Wnt/beta-Catenin Pathway by Promoting Dishevelled Ubiquitination/Degradation in Liver Cancer [1].
• A band of EBV infected, koilocyte-like cells is present in the upper part of the prickle cell layers, these cells being swollen and pale staining, with prominent cell borders and perinuclear vacuoles [2].
• Atypical lymphocytes with deep nuclear indentations, identical to those observed in Sézary syndrome and mycosis fungoides, were demonstrated by electron microscopy in the prickle-cell layer of the oral epithelium of patients with Behçet's syndrome [3].
• The virion antigens were detected in the prickle cell, granular and keratin layers [4].
• Indirect immunofluorescent staining of cryostat sections of human tissues demonstrated an intense nuclear fluorescence in cells of the prickle cell layer of condylomata acuminata sections [5].

High impact information on PRICKLE1

• Clinicopathologic analysis showed that underexpression of Prickle-1 was significantly associated with overexpression of Dvl3, beta-catenin accumulation (P = .023), and larger tumor size (P = .030) [1].
• Facial cell soma migration defects were associated with the coordinate downregulation of multiple components of the planar cell polarity pathway including Fzd7, Wnt11, Prickle1, Vang1 and Vang2 [6].
• A recent study shows that, in ascidians, the planar cell polarity gene prickle regulates sequential establishment of cell polarity during two phases of notochord morphogenesis [7].
• E-cadherin was found throughout the epithelium but was weakly expressed at the basal aspect of the basal cells layer and showed strong positivity in the prickle cell and squamous cell layers [8].
• By using an antibody raised in rabbits against the N-terminal portion of the molecule, the polypeptide may be demonstrated in cells of the prickle cell layer of normal skin and in the cells of hair follicles [9].

Chemical compound and disease context of PRICKLE1

• BrdU-positive cells were localized in the basal layer in both normal and hyperplastic epithelium, whereas they were distributed from the basal to the prickle cell layer in squamous cell carcinoma (SCC) [10].
• Cyclosporin-induced gingival hyperplasia: an ultrastructural study of the oral epithelial prickle cells [11].

Biological context of PRICKLE1

• CPNE8, PRICKLE1, Q6ZUQ4 and TUBA8 were mapped to the interval for pig AMC between microsatellites SW152 and SW904 [12].
• In the mutant aimless (aim), which carries a deletion in pk, notochord morphogenesis is disrupted, and cell polarization is lost [13].
• After day 18 of gestation, the Env protein was detected in the prickle layer of the esophageal epithelium of transgenic rats [14].
• Such dark prickle cells showed characteristic findings of apoptosis, such as the shrinkage of nucleus and cytoplasm and the formation of contraction vacuoles [15].

Anatomical context of PRICKLE1

• We report that the putative PCP protein Prickle-like 2 (Pk2) is distributed in crescents on the medial sides of vestibular epithelial cells before the morphological polarization of hair cells [16].
• Asymmetric distribution of Prickle-like 2 reveals an early underlying polarization of vestibular sensory epithelia in the inner ear [16].
• Ascidian prickle regulates both mediolateral and anterior-posterior cell polarity of notochord cells [13].
• Desmosomes are most frequent in the prickle cell layer, where desmosome fields may occur, and in the lower functional cell layer [17].
• In tissue sections of normal epithelium from the cervix uteri and the oral cavity, the maturing keratinocytes in the prickle-cell layers were moderately or strongly stained when antiserum against CRBP was used, while the proliferating cells in the basal-cell layer were stained only lightly if at all [18].

Associations of PRICKLE1 with chemical compounds

• Much glycogen was present in the cytoplasm of the prickle and functional cell layers as demonstrated by PAS (and diastase digestion) techniques [19].
• In this study the ultrastructural characteristics of the prickle cells of the human gingival epithelium after cyclosporin-A treatment are described [11].
• This would allow basal, prickle, and granular keratinocytes to respond to acetylcholine differently, in accordance with their functions at each stage of keratinocyte development in epidermis [20].
• Filaggrin- and involucrin-positive layers were expanded, particularly the latter, down to the lower prickle cell layer [21].

Regulatory relationships of PRICKLE1

• In nasal polyp tissues, IL-17 was expressed mainly in the cytoplasm of plasma cells and to a lesser degree in the prickle cell layer of the epithelium and the acinus of the serous gland [22].

Other interactions of PRICKLE1

• Enforced expression of Prickle-1 significantly reduced the Wnt/beta-catenin activity and tumorigenic properties of HCC cells [1].
• RUNX3 expression was shown in prickle and functional cell layer cells in normal esophageal mucosa [23].
• METHODS AND RESULTS: In the normal esophageal mucosa, CD55 predominantly stained on the cell membrane of squamous epithelium in the superficial and prickle cell layers, whereas CD46 most intensely stained on the cell membrane in the basal and parabasal cell layers [24].
• RESULTS: In the cholesteatoma epithelium specimens, cdk2 and cdk4 were observed to be expressed in the basal and parabasal layers and in the upper layer (prickle layer and granular layer) [25].
• In normal epidermis, the largest proportion of PCNA- and Ki-67-positive cells was observed in the basal cell layer, with the amounts decreasing through the suprabasal cell layer towards the prickle cell layer [26].

Analytical, diagnostic and therapeutic context of PRICKLE1

• Neural correlates of prickle sensation: a percept-related fMRI study [27].
• Subjects consistently reported an intense, brief jab of prickle at both hairy and glabrous sites during the rewarming phase [28].
• Transcutaneous electrical stimulation and the sensation of prickle [29].
• In situ hybridization revealed a comparable pattern of mRNA distribution for K4 and K13, with expression restricted to parabasal and lower prickle cells [30].
• Painful pricks and prickle pains: is there a relation between children's ratings of venipuncture pain and parental assessments of usual reaction to other pains [31]?

References