Phosphorylation of liver gap junction protein by protein kinase C

Takeda, Atsushi; Hashimoto, Eikichi; Yamamura, Hirohei; Shimazu, Takashi

doi:10.1016/0014-5793(87)81330-3

Cited by 90 publications

(35 citation statements)

References 18 publications

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“…Support for the latter hypothesis is provided by the demonstration that Cx32 (Saiez et al, 1986(Saiez et al, , 1990Takeda et al, 1987Takeda et al, , 1989Traub et al, 1987Traub et al, , 1989, Cx43 (Crow et al, 1990;Musil et al, 1990a,b;Kadle et al, 1991;Laird et al, 1991;Lau et al, 1991;Berthoud et al, 1992), and Cx45 Traub et al, 1995) are phosphoproteins. In contrast, Cx26 has no obvious consensus sites for phosphorylation (Zhang and Nicholson, 1989), and is not phosphorylated in hepatocytes or in isolated liver gap junctions incubated with ATP and the catalytic subunit of cAMP-dependent protein kinase, protein kinase C (PKC), or Ca2+/calmodulin-dependent protein kinase II (Traub et al, 1989;Saez et al, 1990).…”

Section: Introductionmentioning

confidence: 75%

“…This idea is further strenghtened by preliminary results from experiments performed on SKHepl cells stably transfected with a cDNA coding for rat Cx32. Although a PKC-mediated phosphorylation of Cx32 has been demonstrated (Takeda et al, 1987;Saez et al, 1990), TPA did not change the extent of dye coupling nor the frequency distribution of Cx32 conductances (-60 pS) in these SKHepl/Cx32 cells (Chanson, Kwak, and Hermans, unpublished results).…”

Section: Expression Of Protein Kinasesmentioning

confidence: 99%

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Differential regulation of distinct types of gap junction channels by similar phosphorylating conditions.

Kwak

Hermans

Jonge

et al. 1995

MBoC

161

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Under control conditions, the distinct types of gap junction channels could be distinguished on the basis of their permeability and single channel properties. Under various phosphorylating conditions, these channels behaved differently. Whereas agonists/antagonist of PKA did not affect permeability and conductance of all gap junction channels, variable changes were observed under PKC stimulation. Cx45 channels exhibited an additional conductance state, the detection of the smaller conductance states of Cx43 channels was favored, and Cx26 channels were less often observed. In contrast to the other kinases, agonists/antagonist of PKG affected permeability and conductance of Cx43 gap junction channels only. Taken together, these results show that distinct types of gap junction channels are differentially regulated by similar phosphorylating conditions. This differential regulation may be of physiological importance during modulation of cell-to-cell communication of more complex cell systems.

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Section: Introductionmentioning

confidence: 75%

Section: Expression Of Protein Kinasesmentioning

confidence: 99%

Differential regulation of distinct types of gap junction channels by similar phosphorylating conditions.

Kwak

Hermans

Jonge

et al. 1995

MBoC

161

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“…These observations suggest that in certain cells the src gene product and PMA can directly or indirectly interfere with intercellular communication through a cellular protein kinase (15), although studies by Saez et al (40) imply that there are several mechanisms by which intercellular junctional communication can be inhibited. The recent demonstration that protein kinase C, an enzyme activated by tumor promoters such as PMA, can phosphorylate liver gap-junction proteins provides further suggestive evidence for the role of intercellular junctions in carcinogenesis (41).…”

Section: Resultsmentioning

confidence: 99%

Loss of intercellular junctional communication correlates with metastatic potential in mammary adenocarcinoma cells.

Nicolson

Dulski

Trosko

1988

Proc. Natl. Acad. Sci. U.S.A.

106

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A series of rat 13762NF mammary adenocarcinoma cell sublines and clones of various spontaneous pulmonary metastatic potentials from the mammary fat pads of syngeneic rats were examined for their intercellular junctional communication. Using the scrape-loading dye-transfer technique to introduce Lucifer yellow (Mr 457) into cells, we measured the abilities of 13762NF cells to transfer dye to adjacent cells. There was an excellent correlation between loss of Lucifer yellow dye transfer and spontaneous metastatic potential (average total volume of lung metastases inversely correlated to % cells coupled, r = 0.93; average total number of lung metastases inversely correlated to % cells coupled, r = 0.91). The data suggest that high metastatic potentials are closely correlated with loss of intercellular junctional communication in these malignant mammary tumor cells. (25). Rhodamine dextran (Mr 10,000) is used as a control dye, because it cannot diffuse through intact cell membranes or gap junctions (26). When added simultaneously, the two dyes can be used to verify that dye transfer occurs through intercellular junctions (24). Several studies have demonstrated that such dye transfer is related to the morphological presence of gap junctions, radioactive metabolite transfer, and electrical coupling between cells (24, 27-29). RESULTSExamination of 13762NF cell clones revealed that cells of nonmetastatic or low metastatic potential (MTC.4 and MTPa, respectively) were completely coupled; after confluent cultures of the cells were scrape-loaded, they all transferred Lucifer yellow to adjacent cells (Fig. la). Tumor cells of intermediate metastatic potential (MTF7) showed less coupling than cells of low metastatic potential (Fig. ic), and highly metastatic cells (MTLn3) were completely uncoupled (Fig. le). As in previous experiments (23,28), rhodamine dextran was not transferred in any of the cultures (data not shown), indicating that the transfer of Lucifer yellow was not nonspecific. Table 1 summarizes the results of six independent experiments (at least 100-200 cells of each cell line or clone were examined in each individual experiment) using Lucifer yellow dye transfer to assess intercellular communication between 13762NF cells. There was an excellent correlation between metastatic potential and loss of intercellular junctional communication (average total volume of metastases inversely correlated to % cells coupled, r = 0.93; average number of metastases inversely correlated to % cells coupled, r = 0.91). In addition, when grown subcutaneously as tumors in the mammary fat pads of F344 rats, nonmetastatic MTC.4 but not highly metastatic Abbreviation: PMA, phorbol 12-myristate 13-acetate. 473The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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“…One effect ofprotein kinase C is the phosphorylation of a 27 kd gap junction protein (180). Treatment of cells with CAMP blocked the TPA-induced reorganization of the cytoskeleton (154) …”

Section: Cohimunicationmentioning

confidence: 99%

Intercellular Communication in Bronchial Epithelial Cells: Review of Evidence for a Possible Role in Lung Carcinogenesis

et al. 1990

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A challenging aspect of lung carcinogenesis is the elucidation of the mechanisms which permit initiated bronchial epithelial cells to attain a growth advantage over normal bronchial epithelial cells, and subsequently evolve into a malignant phenotype. In this review, the effects of interactions between normal and transformed cells, and the potential role of representative extrinsic factors on cell-cell communication are discussed. Evidence is presented to show how cell injury and the effects of serum and calcium may affect morphology and communication, and tumor development. A large number of autocrine-paracnne factors (e.g., TGFp, TGFa) are released by bronchial epithelial cells. These factors may inhibit or promote the proliferation of normal and transformed bronchial epithelial cells, respectively. The ability of certain injurious and tumor promoting agents (e.g., formaldehyde, TPA) to select for the transformed phenotype may involve selective cell injury, the induction of terminal differentiation and an inhibition of gap junction communication among normal BE cells.

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Phosphorylation of liver gap junction protein by protein kinase C

Cited by 90 publications

References 18 publications

Differential regulation of distinct types of gap junction channels by similar phosphorylating conditions.

Differential regulation of distinct types of gap junction channels by similar phosphorylating conditions.

Loss of intercellular junctional communication correlates with metastatic potential in mammary adenocarcinoma cells.

Intercellular Communication in Bronchial Epithelial Cells: Review of Evidence for a Possible Role in Lung Carcinogenesis

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