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The protein encoded by RECK is a cysteine-rich, extracellular protein with protease inhibitor-like domains whose expression is suppressed strongly in many tumors and cells transformed by various kinds of oncogenes. Additionally we are shipping RECK Kits (10) and RECK Proteins (4) and many more products for this protein.
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Human Polyclonal RECK Primary Antibody for IF (cc), IF (p) - ABIN681418
Siddesha, Valente, Sakamuri, Gardner, Delafontaine, Noda, Chandrasekar: Acetylsalicylic acid inhibits IL-18-induced cardiac fibroblast migration through the induction of RECK. in Journal of cellular physiology 2014
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Results report that the expression of RECK is significantly lower in cervical cancer cells than in normal cells. The relative protein expression levels of p53 (show TP53 Antibodies) signaling (p21 (show CDKN1A Antibodies) and Bax (show BAX Antibodies)) were significantly elevated when RECK was upregulated, suggesting that the overexpression of RECK could promote the activation of p53 (show TP53 Antibodies) signaling pathway.
The expression of RECK was inhibited by the transfection of miR (show MLXIP Antibodies)-96 mimics. RECK mRNA level was reduced by miR (show MLXIP Antibodies)-96 mimics and increased by miR (show MLXIP Antibodies)-96 inhibitor. In the invasion assay, miR (show MLXIP Antibodies)-96 mimics were shown to promote tumor invasion.
Results suggested that some paracrine substances produced by 786-0 cells may reduce RECK expression of adjacent HMEC-1 cells and enhance their proliferation and in vitro angiogenic capacity.
RECK gene polymorphisms were closely associated with active proliferation, capsular invasion, and clinical recurrence of ameloblastoma.
Collectively, these results demonstrated that IL-32alpha upregulates the atheroprotective genes Timp3 (show TIMP3 Antibodies) and Reck by downregulating microRNA-205 through regulation of the Rprd2-Dgcr8 (show DGCR8 Antibodies)/Ddx5 (show DDX5 Antibodies)-Dicer1 (show DICER1 Antibodies) biogenesis pathway.
RECK CpG methylation pattern may predict prognosis and drug-sensitivity of breast cancers.
The expression of RECK in human healthy and diseased gingiva may contribute to periodontal physiological and pathological processes; low RECK expression may be associated with the enhanced MMP-2 (show MMP2 Antibodies) and MMP-9 (show MMP9 Antibodies) production in inflamed gingiva.
the RECK gene polymorphism influences molecular carcinogenesis and clinic pathological features of hepatocellular carcinoma within the Egyptian population
Reversion-inducing, cysteine-rich protein (show SPARC Antibodies) with kazal motifs (RECK) was identified as the direct and functional target of miR (show MLXIP Antibodies)-92b in osteosarcoma
RECK expression in uterine leiomyoma is negatively regulated by miR (show MLXIP Antibodies)-15b.
Reck was identified to be one of the target genes of miR (show MLXIP Antibodies)-497-5p, and Reck could suppress the expression of matrix metalloproteinase-2 (Mmp2 (show MMP2 Antibodies)) and Mmp9 (show MMP9 Antibodies), which could activate latent transforming growth factor-beta1 (TGF-beta1 (show TGFB1 Antibodies)).
experiments indicate that Reck and Gpr124 (show GPR124 Antibodies) are part of the cell surface protein (show CD28 Antibodies) complex that transduces Wnt7a (show WNT7A Antibodies)- and Wnt7b (show WNT7B Antibodies)-specific signals in mammalian CNS Epithelial Cells to promote angiogenesis and regulate the BBB (show ALMS1 Antibodies).
These findings demonstrate the importance of appropriate cell-cell interactions and ECM (show MMRN1 Antibodies) maintenance for angiogenesis and the involvement of Reck as a critical regulator of these events.
RECK-mediated beta1-Integrin regulation by TGF-beta1 (show TGFB1 Antibodies) is critical for wound contraction in mice.
MiR (show MLXIP Antibodies)-21 modulated the osteoporosis by targeting RECK.
microRNA-200b and microRNA-200c promote colorectal cancer cell proliferation via targeting RECK.
The RECK silencing-EGFR (show EGFR Antibodies)-HIF-2alpha (show EPAS1 Antibodies) axis might be a key molecular mechanism to induce hyperplastic phenotype of epithelial cells.
Angiotensin II suppresses RECK, but induces matrix metalloproteinases both in vivo and in vitro.
therapeutic concentrations of ASA (show ARSA Antibodies) inhibited IL-18 (show IL18 Antibodies)-induced H(2)O(2) generation, MMP9 (show MMP9 Antibodies) activation, RECK suppression, and CF migration.
these data suggest that RECK is a novel transcriptional target of FXR (show NR1H4 Antibodies) in mouse liver, and provide clues to better understanding the function of FXR (show NR1H4 Antibodies) in liver.
The protein encoded by this gene is a cysteine-rich, extracellular protein with protease inhibitor-like domains whose expression is suppressed strongly in many tumors and cells transformed by various kinds of oncogenes. In normal cells, this membrane-anchored glycoprotein may serve as a negative regulator for matrix metalloproteinase-9, a key enzyme involved in tumor invasion and metastasis.
membrane-anchored glycoprotein (metastasis and invasion)
, reversion-inducing cysteine-rich protein with Kazal motifs
, suppression of tumorigenicity 15 (reversion-inducing-cysteine-rich protein with kazal motifs)
, suppression of tumorigenicity 5 (reversion-inducing-cysteine-rich protein with kazal motifs)
, suppressor of tumorigenicity 15 protein
, Reversion-inducing cysteine-rich protein with Kazal motifs precursor (mRECK)
, membrane-anchored glycoprotein RECK
, suppression of tumorigenicity 15
, reversion-inducing-cysteine-rich protein with Kasal motifs