K. Laughlin

发表

Increased Tight Junction Permeability Can Result from Protein Kinase C Activation/Translocation and Act as a Tumor Promotional Event in Epithelial Cancers

J. M. Mullin, N. Ginanni, A. Peralta Soler, 2000, Annals of the New York Academy of Sciences.

Modulation of tumor necrosis factor-induced increase in renal (LLC-PK1) transepithelial permeability.

L. M. Russo, A. P. Soler, C. Marano, 1992, The American journal of physiology.

Sodium-independent carrier-mediated inositol transport in cultured renal epithelial (LLC-PK1) cells.

L. M. Russo, C. Marano, J. M. Mullin, 1995, Biochimica et biophysica acta.

Long‐term effects of tumor necrosis factor on LLC‐PK1 transepithelial resistance

L. M. Russo, A. P. Soler, C. Marano, 1993, Journal of cellular physiology.

Chronic exposure of LLC-PK1 epithelia to the phorbol ester TPA produces polyp-like foci with leaky tight junctions and altered protein kinase C-alpha expression and localization.

L. M. Russo, A. P. Soler, J. M. Mullin, 1996, Experimental cell research.

Protein kinase C activation increases transepithelial transport of biologically active insulin.

J. M. Mullin, N. Ginanni, K. Laughlin, 1998, Cancer research.

Overexpression of protein kinase C-δ increases tight junction permeability in LLC-PK1epithelia.

Z. Szallasi, B. Kachar, R. Miller, 1998, American journal of physiology. Cell physiology.

Overexpression of protein kinase C- (cid:100) increases tight junction permeability in LLC-PK 1 epithelia

Z. Szallasi, B. Kachar, R. Miller, 1998 .

Different size limitations for increased transepithelial paracellular solute flux across phorbol ester and tumor necrosis factor‐treated epithelial cell sheets

A. P. Soler, C. Marano, J. M. Mullin, 1997, Journal of cellular physiology.

Transepithelial paracellular leakiness induced by chronic phorbol ester exposure correlates with polyp-like foci and redistribution of protein kinase C-alpha.

A. P. Soler, J. M. Mullin, K. Laughlin, 1997, Carcinogenesis.

Increased tight junctional permeability is associated with the development of colon cancer.

R. Miller, A. P. Soler, J. M. Mullin, 1999, Carcinogenesis.

The transient increase of tight junction permeability induced by bryostatin 1 correlates with rapid downregulation of protein kinase C-alpha.

J. M. Mullin, N. Ginanni, G. Pettit, 2000, Experimental cell research.

Effects of epidermal growth factor versus phorbol ester on kidney epithelial (LLC-PK1) tight junction permeability and cell division.

A. P. Soler, J. M. Mullin, K. Laughlin, 1993, Experimental cell research.

Plasma concentrations of soluble tumor necrosis factor receptor I and tumor necrosis factor during cardiopulmonary bypass.

G. Reichard, S. Goldman, C. Marano, 2000, The Annals of thoracic surgery.

The protein kinase C inhibitor, bisindolylmaleimide, inhibits the TPA-induced but not the TNF-induced increase in LLC-PK1 transepithelial permeability.

L. M. Russo, C. Marano, J. M. Mullin, 1995, Biochemical and biophysical research communications.

Overexpression of protein kinase C-delta increases tight junction permeability in LLC-PK1 epithelia.

Z. Szallasi, B. Kachar, R. Miller, 1998, The American journal of physiology.

LETTER: ELECTROPHYSIOLOGICAL DIFFERENCES IN NORMAL COLON MUCOSA FROM DIVERTICULAR DISEASE VS CANCER

J. Schulzke, J. M. Mullin, J. Thornton, 2000, Digestive Diseases and Sciences.