Disease relevance of Blister

• In this series of patients, cutaneous lesions included discoid lupus erythematosus, lichen planus, vitiligo, chronic bullous lesions of the legs, and scleroderma [1].
• Whereas the vesicular stomatitis virus G protein and the influenza virus hemagglutinin were uniformly distributed on the surface of untreated cells, in CB-treated cells, they were strikingly concentrated at cell extremities in the regions of clustered blebs [2].
• Because development of a pneumothorax and/or pulmonary blebs may be the earliest or the only clinical manifestation of FLCN mutations, pulmonologists should be alert to the contribution of this gene toward this familial form of emphysema [3].
• Most mutations in FLCN cause a rare disease, Birt-Hogg-Dubé syndrome, characterized by autosomal dominant inheritance of multiple benign skin lesions, renal tumors, pulmonary blebs, and pneumothoraces [3].
• The effects of lowering subretinal Ca2+ concentration in living rabbit eyes was investigated by making experimental retinal detachments (blebs) filled with Ca(2+)-free disodium edetate solution [4].

High impact information on Blister

• Identification of a new gene mutated in Fraser syndrome and mouse myelencephalic blebs [5].
• Mutant DRP-1 causes the mitochondrial matrix to retract into large blebs that are both surrounded and connected by tubules of outer membrane [6].
• However, the alpha3 domain plays a key role in transducing the death signal, which mediates extensive aggregation of the MHC class I-integrin-actin filament system, giving rise to membrane blebs and pores [7].
• The clustering of the autoantigens targeted in systemic lupus erythematosus within surface blebs of apoptotic cells generates high concentrations of autoantigen within discrete subcellular packages [8].
• The larger blebs (apoptotic bodies) contain nucleosomal DNA, Ro, La, and the small nuclear ribonucleoproteins [9].

Chemical compound and disease context of Blister

• There was also an abrupt increase in the release of lactate dehydrogenase and protein after reoxygenation, and cytoplasmic fragments corresponding in size and shape to blebs were recovered by filtration of the effluent perfusate [10].
• In most cells, estradiol and TRH led to an increase in the number and prominence of microvilli and blebs, whereas CB-154 treatment resulted in a slightly decreased number of microvilli and an increased occurrence of membrane foldings [11].
• On blebs, acetylcholine receptors, concanavalin A receptors, and stearoyldextran extrinsic model receptor molecules are free to diffuse with a diffusion coefficient (D) approximately 3 x 10(-9) cm2/s, which is close to the value predicted for hydrodynamic drag in the lipid membrane [12].
• Lipid analog diffusion is also slightly enhanced in blebs as expected of evanescent lipid protein interaction [12].
• The rapid response to dapsone therapy suggests that dapsone is useful in treating bullous lesions of systemic lupus erythematosus [13].

Biological context of Blister

• In the present study, a model system is described for using the caspase inhibitor, z-VAD-FMK, to block apoptosis and generate a synchronous population of cells actively extruding and retracting membrane blebs [14].
• Tissue morphogenesis and vascular stability require the Frem2 protein, product of the mouse myelencephalic blebs gene [15].
• The mutant prelamin A in HGPS, which is commonly called progerin, retains the CAAX motif that triggers farnesylation, but the 50-aa deletion prevents the subsequent processing to mature lamin A. The presence of progerin adversely affects the integrity of the nuclear lamina, resulting in misshapen nuclei and nuclear blebs [16].
• Hepatotoxicity of the herbal medicine germander: metabolic activation of its furano diterpenoids by cytochrome P450 3A Depletes cytoskeleton-associated protein thiols and forms plasma membrane blebs in rat hepatocytes [17].
• The level of tyrosine phosphorylation of cortactin is correlated with the formation of membrane blebs [18].

Anatomical context of Blister

• Corneal epithelium removed from underlying extracellular matrix (ECM) extends numerous cytoplasmic processes (blebs) from the formerly smooth basal surface [19].
• Immunofluorescence localization studies further reveal that, in contrast to the distribution of caldesmon along actin stress fibers in normal fibroblasts, caldesmon colocalizes with Shc in plasma membrane blebs in transformed fibroblasts [20].
• Furthermore, Frem1 appears to act as a dermal mediator of basement membrane adhesion, apparently independently of the other known "blebs" proteins Fras1 and Grip1 [21].
• Scanning electron micrographs of target cells from cis-DDP treated rats showed certain morphological features (cell surface blebs and the appearance of giant cells) that were not found in control target cell populations [22].
• Apoptotic and necrotic blebs elicited by H(2)O(2) were compared in terms of dynamics, structure and underlying biochemistry in HeLa cells and Clone 9 cells [23].

Gene context of Blister

• Here we report the identification of mutations in an extracellular matrix gene Fras1-related extracellular matrix gene 1 (Frem1) in both the classic head blebs mutant and in an N-ethyl-N-nitrosourea-induced allele [21].
• Cells lacking TEL2 function died, with some cells arresting as large cells with three or four small protrusions or "blebs."[24]
• In embryos from RhoGEF2 or dia germline clones, furrow canals do not form at all or are considerably enlarged and contain cytoplasmic blebs [25].
• CD7 and CD43 colocalized in small patches away from the membrane blebs, which excluded externalized phosphatidylserine [26].
• CD45 and CD3 colocalized on large islands on apoptotic blebs protruding from the cell surface [26].

Analytical, diagnostic and therapeutic context of Blister

• When examined by light and electron microscopy, cells stored in both University of Wisconsin solution and Hanks' HEPES buffer for 24 hr appeared essentially normal except for the presence of numerous membrane blebs in the Hanks' HEPES buffer group [27].
• Using confocal microscopy, we found that DR5, caspase-8, and caveolin-1 became progressively concentrated in blebs of plasmalemma as they formed in response to TRAIL [28].
• 2. Injection of either a Ca2+ chelator or 3',5'-cyclic AMP slowed or halted shortening and promoted re-extension of a cell or collapse of membrane evaginations (blebs) in a manner similar to that following cessation of electrical stimulation [29].
• Intravenous injection of hyperosmotic solution (mannitol) accelerated the resorption of Hanks'-filled blebs but the injection of hypoosmotic solution (water) had no clear effect [30].
• TGF-beta concentration in blebs formed around the xenografts (but not in the serum) was higher in animals that underwent transplantation with MMC-treated islets than with untreated islets [31].

References