Life (and death) in the Fas lane

Akbar, AN

doi:10.1136/gut.43.1.5

Cited by 5 publications

(3 citation statements)

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“…Binding of Fas‐L or agonistic anti‐Fas antibodies to Fas induces apoptosis and an energy‐dependent cascade begins on the cell membrane. This system regulates immune and inflammatory responses 1,2 , 4,11 , 12,26–31 …”

Section: Introductionmentioning

confidence: 99%

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Expression of Fas, Bcl‐2 and p53 molecules in glomerulonephritis and their correlations with clinical and laboratory findings*

et al. 2005

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Section: Introductionmentioning

confidence: 99%

“…This system regulates immune and inflammatory responses. 1,2,4,11,12,[26][27][28][29][30][31] Bcl-2 is a protein that inhibits apoptosis regulated by mitochondrial functions. 17,[32][33][34] Bcl-2 overexpression might play a role in the prolonged proliferation of mesangial cells and glomerular hypercellularity in glomerulo-nephritis.…”

Section: Introductionmentioning

confidence: 99%

Expression of Fas, Bcl‐2 and p53 molecules in glomerulonephritis and their correlations with clinical and laboratory findings*

et al. 2005

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“…It was therefore cautioned that the mere expression of CD95 within colonic epithelium together with increased CD95L expression does not necessarily indicate CD95-induced apoptosis. 58 • More recent studies did not find a correlation between CD95L expression and apoptosis or inflammation during active colitis. In contrast, perforin expression did correlate with apoptosis.…”

Section: Cd95 In Uc: Yesterday and Todaymentioning

confidence: 96%

Cell death in the colonic epithelium during inflammatory bowel diseases

Chen¹,

Park²,

Turner³

et al. 2010

Inflammatory Bowel Diseases

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CD95 is a member of the death receptor family. It is a prototypical inducer of apoptosis that, upon binding of its cognate ligand (CD95L), forms a death-inducing signaling complex composed of adaptor molecules and initiator caspases that transmit the apoptosis signal. The CD95/CD95L system was implicated in the etiology of inflammatory bowel disease (IBD) based, primarily, on the finding that CD95 is highly expressed in the intestinal epithelial cells and that epithelial apoptosis is increased in IBD. In recent years it has been recognized that CD95, while playing an important role as an apoptosis-inducing receptor in the immune system, also has multiple nonapoptotic functions on nonimmune cells. This review critically discusses the data on the possible function of CD95 as an apoptosis-inducing receptor in IBD and discusses alternative mechanisms for epithelial cell loss in IBD.

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