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TIMP metallopeptidase inhibitor 3

TIMP-3, Tissue Inhibitor of Metalloproteinase-3, tissue inhibitor of metalloproteinases-3
This gene belongs to the TIMP gene family. The proteins encoded by this gene family are inhibitors of the matrix metalloproteinases, a group of peptidases involved in degradation of the extracellular matrix (ECM). Expression of this gene is induced in response to mitogenic stimulation and this netrin domain-containing protein is localized to the ECM. Mutations in this gene have been associated with the autosomal dominant disorder Sorsby's fundus dystrophy. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: MMP-2, MMP-9, HAD, TIMP-2, CAN
Papers using TIMP-3 antibodies
Evaluation of a Photographic Chondropathy Score (PCS) for pathological samples in a study of inflammation in tibiofemoral osteoarthritis
Walsh D.A. et al., In Osteoarthritis and Cartilage, 2008
... Monoclonal anti-TIMP-3 (clone 136-13H4) was from Merck, Nottingham, UK ...
Papers on TIMP-3
TIMP3 regulates osteosarcoma cell migration, invasion, and chemotherapeutic resistances.
Tang et al., Shanghai, China. In Tumour Biol, Feb 2016
Low levels of TIMP3 have been demonstrated in cancer tissues at advanced clinical stages, with positive distant metastasis and chemotherapeutic resistance.
Hepatoprotective Effects of Traditional Chinese Medicine on Liver Fibrosis from Ethanol Administration following Partial Hepatectomy.
Huang et al., China. In Chin J Physiol, Jan 2016
Cyclin D1, MMP-2, MMP-9, TIMP-1, TIMP-2 and TIMP-3 mRNA by RT-PCR were analyzed in cirrhotic fibrosis rats.
The Ezh2 polycomb group protein drives an aggressive phenotype in melanoma cancer stem cells and is a target of diet derived sulforaphane.
Eckert et al., Baltimore, United States. In Mol Carcinog, Jan 2016
A375 melanoma cell-derived MCS cells form rapidly growing tumors in immune-compromised mice and SFN treatment of these tumors reduces tumor growth and this is associated with reduced Ezh2 level and H3K27me3 formation, reduced matrix metalloproteinase expression, increased TIMP3 expression and increased apoptosis.
A large genome-wide association study of age-related macular degeneration highlights contributions of rare and common variants.
Heid et al., Ann Arbor, United States. In Nat Genet, Jan 2016
Very rare coding variants (frequency <0.1%) in CFH, CFI and TIMP3 suggest causal roles for these genes, as does a splice variant in SLC16A8.
Association of TIMP3 expression with vessel density, macrophage infiltration and prognosis in human malignant melanoma.
Ten Hagen et al., Rotterdam, Netherlands. In Eur J Cancer, Jan 2016
AIMS: Several anti-tumour properties have been ascribed to the tissue inhibitor of matrix metalloproteinases-3 (TIMP3) gene, including inhibition of neovascularisation in tumour xenografts.
[Expression and pathological mechanism of MMP-9 and HIF-2α in CD133(+) lung cancer stem cells].
Sun et al., Suzhou, China. In Zhonghua Yi Xue Za Zhi, Sep 2015
Real-time polymerase chain reaction (PCR) was used for the investigation of expression of tumor metastasis associated genes, including MMP-1, MMP-2, MMP-9, HIF-1α, HIF-1β, HIF-2α and tissue inhibitor of metalloproteinase (TIMP)-1, TIMP-2, TIMP-3, TIMP-4.
Signalling in inflammatory skin disease by AP-1 (Fos/Jun).
Wagner et al., Madrid, Spain. In Clin Exp Rheumatol, Jul 2015
In this GEMM and in psoriasis patient-derived material, S100A8/A9-dependent C3/CFB complement activation, as well as a miR-21-dependent TIMP-3/TACE pathway leading to TNF-α shedding, plays causal roles in disease development.
Effect of tissue inhibitor of metalloproteinases 3 on DLK1 shedding in cultured human pre-adipocytes and implications for adipose tissue remodelling.
Turner et al., Norwich, United Kingdom. In Lancet, Mar 2015
We hypothesised that in health, tissue inhibitor of metalloproteinases 3 (TIMP3) modulates adipose tissue remodelling by regulating extracellular matrix turnover and shedding of the adipogenic regulator DLK1, but that in adipose tissue inflammation it might drive development of metabolically unhealthy obesity.
The role of metalloproteinases and their tissue inhibitors in adipose tissue remodelling and whole-body lipid distribution: a cross-sectional clinical study.
Turner et al., Norwich, United Kingdom. In Lancet, Mar 2015
Subcutaneous adipose tissue TIMP3 expression correlated with subcutaneous adipocyte area (r=0·72, p=0·029), but not with HOMA2-IR (r=-0·53, p=0·062).
Can Novel Treatment of Age-Related Macular Degeneration Be Developed by Better Understanding of Sorsby's Fundus Dystrophy.
Chong et al., Oxford, United Kingdom. In J Clin Med, 2014
Sorsby's Fundus Dystrophy (SFD) is a rare autosomal dominant maculopathy that shares many clinical features with Age-Related Macular Degeneration (AMD).
MiR-21: an environmental driver of malignant melanoma?
Melnik, Osnabrück, Germany. In J Transl Med, 2014
MiR-21 is an oncomiR that affects critical target genes of malignant melanoma, resulting in sustained proliferation (PTEN, PI3K, Sprouty, PDCD4, FOXO1, TIPE2, p53, cyclin D1), evasion from apoptosis (FOXO1, FBXO11, APAF1, TIMP3, TIPE2), genetic instability (MSH2, FBXO11, hTERT), increased oxidative stress (FOXO1), angiogenesis (PTEN, HIF1α, TIMP3), invasion and metastasis (APAF1, PTEN, PDCD4, TIMP3).
Role of flow-sensitive microRNAs in endothelial dysfunction and atherosclerosis: mechanosensitive athero-miRs.
Jo et al., Atlanta, United States. In Arterioscler Thromb Vasc Biol, 2014
Furthermore, we have recently shown that the miR-712/205 family, which is upregulated by disturbed flow, contributes to endothelial inflammation and vascular hyperpermeability by targeting tissue inhibitor of metalloproteinase-3, which regulates metalloproteinases and a disintegrin and metalloproteinases.
New insights into the diagnosis of nodular goiter.
Parczewski et al., Szczecin, Poland. In Thyroid Res, 2013
hypermethylation of RASSF1A gene and TIMP-3 gene) play an important role in the process of neoplastic transformation of thyreocyte.
Endometrial miR-181a and miR-98 expression is altered during transition from normal into cancerous state and target PGR, PGRMC1, CYP19A1, DDX3X, and TIMP3.
Chegini et al., Gainesville, United States. In J Clin Endocrinol Metab, 2012
miR-98 and miR-181a through their regulatory functions on PGRMC1, PGR, CYP19A1, TIMP3, and DDX3X expression may influence a wide range of endometrial cellular activities during normal menstrual cycle and transition into disease states.
Correlation between BRAF mutation and promoter methylation of TIMP3, RARβ2 and RASSF1A in thyroid cancer.
Hoque et al., Baltimore, United States. In Epigenetics, 2012
In papillary thyroid cancer, significant correlations between the methylation status of the TIMP3 gene and the V600E BRAF mutation were found.
TACE activation by MAPK-mediated regulation of cell surface dimerization and TIMP3 association.
Derynck et al., San Francisco, United States. In Sci Signal, 2012
cell signaling altered the dimer-monomer equilibrium and inhibitor association to promote activation of TACE-mediated ectodomain shedding, a regulatory mechanism that may extend to other ADAM proteases.
[Association of the MMP3, MMP9, ADAM33 and TIMP3 genes polymorphic markers with development and progression of chronic obstructive pulmonary disease].
Victorova et al., In Mol Biol (mosk), 2012
The TIMP3 gene polymorphism may be an important risk factor for the development and progression of chronic obstructive pulmonary disease.
[Expressions and significance of TIMP-3 and mtp53 in non-small cell lung cancer].
Zhang et al., Chengdu, China. In Zhongguo Fei Ai Za Zhi, 2012
The expression of TIMP-3 in the non-small cell lung cancer and metastasis groups was downregulated.
miR-221&222 regulate TRAIL resistance and enhance tumorigenicity through PTEN and TIMP3 downregulation.
Croce et al., Columbus, United States. In Cancer Cell, 2010
show that miR-221&222, by targeting PTEN and TIMP3 tumor suppressors, induce TRAIL resistance and enhance cellular migration through the activation of the AKT pathway and metallopeptidases
Quantitative methylation-specific polymerase chain reaction gene patterns in urine sediment distinguish prostate cancer patients from control subjects.
Sidransky et al., Baltimore, United States. In J Clin Oncol, 2005
PATIENTS AND METHODS: We tested urine sediment DNA for aberrant methylation of nine gene promoters (p16INK4a, p14(ARF), MGMT, GSTP1, RARbeta2, CDH1 [E-cadherin], TIMP3, Rassf1A, and APC) from 52 patients with prostate cancer and 21 matched primary tumors by quantitative fluorogenic real-time polymerase chain reaction.
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