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ADAM metallopeptidase domain 12

This gene encodes a member of the ADAM (a disintegrin and metalloprotease) protein family. Members of this family are membrane-anchored proteins structurally related to snake venom disintegrins, and have been implicated in a variety of biological processes involving cell-cell and cell-matrix interactions, including fertilization, muscle development, and neurogenesis. This gene has two alternatively spliced transcripts: a shorter secreted form and a longer membrane-bound form. The shorter form is found to stimulate myogenesis. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: metalloprotease, AGE, CAN, HAD, TACE
Papers on ADAM12
ADAM33 and ADAM12 genetic polymorphisms and their expression in Egyptian children with asthma.
Abdelaziz Almalky et al., Az Zaqāzīq, Egypt. In Ann Allergy Asthma Immunol, Jan 2016
OBJECTIVES: To assess the association between ADAM33 and ADAM12 single-nucleotide polymorphisms (SNPs) with asthma risk and severity and to investigate the effect of ADAM33 and ADAM12 polymorphisms on expression of these proteases in sputum.
The Prediction of the Expected Current Selection Coefficient of Single Nucleotide Polymorphism Associated with Holstein Milk Yield, Fat and Protein Contents.
Kim et al., Seoul, South Korea. In Asian-australas J Anim Sci, Jan 2016
They are phosphodiesterase 4B (PDE4B), serine/threonine kinase 40 (STK40), collagen, type XI, alpha 1 (COL11A1), ephrin-A1 (EFNA1), netrin 4 (NTN4), neuron specific gene family member 1 (NSG1), estrogen receptor 1 (ESR1), neurexin 3 (NRXN3), spectrin, beta, non-erythrocytic 1 (SPTBN1), ADP-ribosylation factor interacting protein 1 (ARFIP1), mutL homolog 1 (MLH1), transmembrane channel-like 7 (TMC7), carboxypeptidase X, member 2 (CPXM2) and ADAM metallopeptidase domain 12 (ADAM12).
Role of hypoxia-related proteins in invasion of ameloblastoma cells: crosstalk between NOTCH1, HIF-1α, ADAM-12, and HB-EGF.
Pinheiro et al., Belém, Brazil. In Histopathology, Jan 2016
Crosstalk between NOTCH1, ADAM-12, HIF-1α and HB-EGF under hypoxic conditions has been implicated in invadopodia formation, tumor invasiveness and metastasis development.
First trimester maternal serum ADAM12-s and PAPP-A levels are altered in pregnancies conceived after assisted reproduction techniques (ART).
Ryynänen et al., Oulu, Finland. In Prenat Diagn, Jan 2016
OBJECTIVE: To estimate whether the maternal serum levels of ADAM12-s, PAPP-A and fβ-hCG are altered in ART pregnancies.
Soluble Delta-like ligand 1 alters human endometrial epithelial cell adhesive capacity.
Dimitriadis et al., In Reprod Fertil Dev, Dec 2015
We also determined the cellular location and immunostaining intensity of ADAM12 and 17 in human endometrium throughout the cycle.
Human Polymorphisms in Placentally Expressed Genes and Their Association With Susceptibility to Congenital Trypanosoma cruzi Infection.
Schijman et al., Salta, Argentina. In J Infect Dis, Dec 2015
We have examined the association of 11 single-nucleotide polymorphisms (SNPs) located in genes coding for placental expression enzymes as genetic markers of susceptibility to congenital T. cruzi infection (hereafter, "congenital infection"): rs2014683 and rs1048988 in ALPP; rs11244787 and rs1871054 in ADAM12; rs243866, rs243865, rs17859821, rs243864, and rs2285053 in MMP2; and rs3918242 and rs2234681 in MMP9.
The role of CDCP1 (CUB domain-containing protein 1) and ADAM12 (a disintegrin and metalloproteinase 12) in ovarian cancer.
Achimas-Cadariu et al., Cluj-Napoca / Kolozsvár, Romania. In J Buon, May 2015
In this view, recent research has been able to highlight promising candidates such as CDCP1 and ADAM12.
The Elsevier Trophoblast Research Award Lecture: Importance of metzincin proteases in trophoblast biology and placental development: a focus on ADAM12.
Beristain et al., Canada. In Placenta, Apr 2015
Specifically, we will discuss the emerging roles that A Disintegrin and Metalloproteinases (ADAMs) play in placental development, with a particular focus on the ADAM subtype, ADAM12.
Early Pregnancy Biomarkers in Pre-Eclampsia: A Systematic Review and Meta-Analysis.
Duvekot et al., Rotterdam, Netherlands. In Int J Mol Sci, 2014
We found low predictive values using individual biomarkers which included a disintegrin and metalloprotease 12 (ADAM-12), inhibin-A, pregnancy associated plasma protein A (PAPP-A), placental growth factor (PlGF) and placental protein 13 (PP-13).
First trimester serum tests for Down's syndrome screening.
Alfirevic et al., Liverpool, United Kingdom. In Cochrane Database Syst Rev, 2014
We evaluated 78 test combinations formed from combinations of 18 different tests, with or without maternal age; ADAM12 (a disintegrin and metalloprotease), AFP (alpha-fetoprotein), inhibin, PAPP-A (pregnancy-associated plasma protein A, ITA (invasive trophoblast antigen), free βhCG (beta human chorionic gonadotrophin), PlGF (placental growth factor), SP1 (Schwangerschafts protein 1), total hCG, progesterone, uE3 (unconjugated oestriol), GHBP (growth hormone binding protein), PGH (placental growth hormone), hyperglycosylated hCG, ProMBP (proform of eosinophil major basic protein), hPL (human placental lactogen), (free αhCG, and free ßhCG to AFP ratio.
ADAM12 expression predicts clinical outcome in estrogen receptor-positive breast cancer.
Mueck et al., Huzhou, China. In Int J Clin Exp Pathol, 2014
OBJECTIVES: Our study was aimed to make sure whether ADAM12 could serve as a prognostic biomarker of estrogen receptor (ER) -positive breast cancer.
Endocrine resistance in breast cancer.
Liu et al., In Climacteric, 2014
Several molecular mechanisms have been proposed to be responsible for endocrine resistance in breast cancer, including MIR-451, FGF and FGFR, ADAM12, fibronectin and other soluble stromal factors, PELP1-KDM1, HER2, NOTCH, δEF1, mTOR, AKT/mTOR, Pi3K/AKT, Pi3K/AKT/mTOR, NFκB, LMTK3, IGF1R, cyclin E2, IRF1, Tab2, and SRC-1.
Lineage tracing and genetic ablation of ADAM12(+) perivascular cells identify a major source of profibrotic cells during acute tissue injury.
Peduto et al., Paris, France. In Nat Med, 2012
Here we show that transient expression of ADAM12 (a disintegrin and metalloprotease 12) identifies a distinct proinflammatory subset of platelet-derived growth factor receptor-α-positive stromal cells that are activated upon acute injury in the muscle and dermis.
[Second trimester screening for trisomy 21 using ADAM12-S as a maternal serum marker].
Xu et al., Nanjing, China. In Zhonghua Yi Xue Yi Chuan Xue Za Zhi, 2012
The median multiple of the median (MoM) value of ADAM12-S in Down Syndrome pregnancy group was higher than that of the control group (P< 0.01).
Upregulated expression of ADAM12 is associated with progression of oral squamous cell carcinoma.
Tanzawa et al., Chiba, Japan. In Int J Oncol, 2012
Data indicate that ADAM12 is overexpressed in oral squamous cell carcinoma and might accelerate cellular proliferation. Its function may be associated with TGF-beta3 signaling.
Constitutive coupling of a naturally occurring human alpha1a-adrenergic receptor genetic variant to EGFR transactivation pathway.
Schwinn et al., Seattle, United States. In Proc Natl Acad Sci U S A, 2012
Data show that elevated levels of matrix metalloproteinase-7 (MMP7) and a disintegrin and metalloproteinase-12 (ADAM12) in alpha(1a)-247R-expressing cells are responsible for EGF receptor (EGFR) transactivation.
The secretion of PAPP-A, ADAM12, and PP13 correlates with the size of the placenta for the first month of pregnancy.
Ryynänen et al., Oulu, Finland. In Placenta, 2011
secretion of PAPP-A, ADAM12 and PP13 is closely related to the size of the placenta in the beginning of pregnancy. After 8 weeks of pregnancy, which is the time for luteoplacental shift, the correlation disappears.
ADAM12 produced by tumor cells rather than stromal cells accelerates breast tumor progression.
Wewer et al., Copenhagen, Denmark. In Mol Cancer Res, 2011
Observation that ADAM12 expression is significantly higher in the terminal duct lobular units adjacent to breast carcinoma compared with TDLUs found in normal breast tissue supports our hypothesis that tumor-associated stroma triggers ADAM12 expression.
ADAM10 is a principal 'sheddase' of the low-affinity immunoglobulin E receptor CD23.
Blobel et al., New York City, United States. In Nat Immunol, 2006
Here we used loss-of-function and gain-of-function experiments with cells lacking or overexpressing candidate CD23-releasing enzymes (ADAM8, ADAM9, ADAM10, ADAM12, ADAM15, ADAM17, ADAM19 and ADAM33), ADAM-knockout mice and a selective inhibitor to identify ADAM10 as the main CD23-releasing enzyme in vivo.
Cardiac hypertrophy is inhibited by antagonism of ADAM12 processing of HB-EGF: metalloproteinase inhibitors as a new therapy.
Higashiyama et al., Ōsaka, Japan. In Nat Med, 2002
We cloned a disintegrin and metalloprotease 12 (ADAM12) as a specific enzyme to shed HB-EGF in the heart and found that dominant-negative expression of ADAM12 abrogated this signaling.
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