PMID- 20303413
OWN - NLM
STAT- MEDLINE
DCOM- 20100927
LR  - 20211020
IS  - 1878-5875 (Electronic)
IS  - 1357-2725 (Print)
IS  - 1357-2725 (Linking)
VI  - 42
IP  - 7
DP  - 2010 Jul
TI  - Tumor necrosis factor-alpha converting enzyme: Implications for ocular 
      inflammatory diseases.
PG  - 1076-9
LID - 10.1016/j.biocel.2010.03.011 [doi]
AB  - Tumor necrosis factor-alpha (TNF-alpha) converting enzyme (TACE), a member of the 
      family of metalloproteinase disintegrin proteins, is responsible for the 
      conversion of inactive TNF-alpha precursor form to active mature form. TNF-alpha 
      is a pleiotropic cytokine that contributes to cellular immunity and inflammatory 
      response in wide range of inflammatory pathologies. Although a large number of 
      studies indicate the use of TACE inhibitors, which prevents processing of 
      TNF-alpha as potential therapeutic drugs for the treatment of inflammatory 
      diseases including rheumatoid arthritis, Crohn's disease and cancer, very few 
      studies indicate its use in ocular pathologies. It is still not clearly 
      understood how the TACE-mediated shedding of cytokines and growth factors in 
      various ocular tissues plays a critical role in the cytotoxic signals causing 
      tissue dysfunction and damage leading to blindness. Regulation of TACE activity 
      is likely to have wide implications for ocular immunology and inflammatory 
      diseases. Specifically, since anti-TNF-alpha therapies have been used to prevent 
      ocular inflammatory complications, the use of TACE inhibitors could be a novel 
      therapeutic approach for ocular inflammatory diseases especially uveitis.
CI  - Copyright 2010 Elsevier Ltd. All rights reserved.
FAU - Ramana, Kota V
AU  - Ramana KV
AD  - Department of Biochemistry and Molecular Biology, University of Texas Medical 
      Branch, 301 University Blvd, Galveston, TX 77555, USA. kvramana@utmb.edu
LA  - eng
GR  - EY018591/EY/NEI NIH HHS/United States
GR  - R01 EY018591/EY/NEI NIH HHS/United States
GR  - R01 GM071036-06/GM/NIGMS NIH HHS/United States
GR  - R01 GM071036/GM/NIGMS NIH HHS/United States
GR  - GM71036/GM/NIGMS NIH HHS/United States
GR  - R01 EY018591-01A2/EY/NEI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
DEP - 20100318
PL  - Netherlands
TA  - Int J Biochem Cell Biol
JT  - The international journal of biochemistry & cell biology
JID - 9508482
RN  - EC 3.4.24.- (ADAM Proteins)
RN  - EC 3.4.24.86 (ADAM17 Protein)
RN  - EC 3.4.24.86 (ADAM17 protein, human)
SB  - IM
MH  - ADAM Proteins/chemistry/*metabolism
MH  - ADAM17 Protein
MH  - Animals
MH  - Enzyme Activation
MH  - Eye/*enzymology/*pathology
MH  - Humans
MH  - Inflammation/*enzymology/pathology
PMC - PMC2880189
MID - NIHMS195441
EDAT- 2010/03/23 06:00
MHDA- 2010/09/29 06:00
PMCR- 2011/07/01
CRDT- 2010/03/23 06:00
PHST- 2010/02/05 00:00 [received]
PHST- 2010/03/10 00:00 [revised]
PHST- 2010/03/11 00:00 [accepted]
PHST- 2010/03/23 06:00 [entrez]
PHST- 2010/03/23 06:00 [pubmed]
PHST- 2010/09/29 06:00 [medline]
PHST- 2011/07/01 00:00 [pmc-release]
AID - S1357-2725(10)00122-6 [pii]
AID - 10.1016/j.biocel.2010.03.011 [doi]
PST - ppublish
SO  - Int J Biochem Cell Biol. 2010 Jul;42(7):1076-9. doi: 
      10.1016/j.biocel.2010.03.011. Epub 2010 Mar 18.