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英文名稱Anti-RECK/FITC
中文名稱FITC標記的金屬蛋白酶抑制因子RECK抗體
別 名hRECK; Membrane anchored glycoprotein (metastasis and invasion); RECK protein; Reversion inducing cysteine rich protein with Kazal motifs; ST15; Suppression of tumorigenicity 15 (reversion inducing cysteine rich protein with kazal motifs); Suppressor of tumorigenicity 15; RECK_HUMAN.
規格100ug
說 明 書100ug
研究領域腫瘤 免疫學 信號轉導 細胞凋亡 轉錄調節因子
抗體來源Rabbit
克隆類型Polyclonal
交叉反應
產品應用ICC=1:50-200 IF=1:50-200
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量107kDa
性 狀Lyophilized or Liquid
濃 度2mg/1ml
免 疫 原KLH conjugated synthetic peptide derived from human RECK
亞 型IgG
純化方法affinity purified by Protein A
儲 存 液0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存條件Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
產品介紹background:
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. 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.
Function:
Negatively regulates matrix metalloproteinase-9 (MMP-9) by suppressing MMP-9 secretion and by direct inhibition of its enzymatic activity. RECK down-regulation by oncogenic signals may facilitate tumor invasion and metastasis. Appears to also regulate MMP-2 and MT1-MMP, which are involved in cancer progression.
Subunit:
Interacts with MMP-9.
Subcellular Location:
Cell membrane; Lipid-anchor, GPI-anchor.
Tissue Specificity:
Expressed in various tissues and untransformed cells. It is undetectable in tumor-derived cell lines and oncogenically transformed cells.
Post-translational modifications:
N-glycosylated.
中文名稱FITC標記的金屬蛋白酶抑制因子RECK抗體
別 名hRECK; Membrane anchored glycoprotein (metastasis and invasion); RECK protein; Reversion inducing cysteine rich protein with Kazal motifs; ST15; Suppression of tumorigenicity 15 (reversion inducing cysteine rich protein with kazal motifs); Suppressor of tumorigenicity 15; RECK_HUMAN.
詳細介紹：
規格100ug
說 明 書100ug
研究領域腫瘤 免疫學 信號轉導 細胞凋亡 轉錄調節因子
抗體來源Rabbit
克隆類型Polyclonal
交叉反應
產品應用ICC=1:50-200 IF=1:50-200
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量107kDa
性 狀Lyophilized or Liquid
濃 度2mg/1ml
免 疫 原KLH conjugated synthetic peptide derived from human RECK
亞 型IgG
純化方法affinity purified by Protein A
儲 存 液0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存條件Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
相關資料：
產品介紹background:
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. 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.
Function:
Negatively regulates matrix metalloproteinase-9 (MMP-9) by suppressing MMP-9 secretion and by direct inhibition of its enzymatic activity. RECK down-regulation by oncogenic signals may facilitate tumor invasion and metastasis. Appears to also regulate MMP-2 and MT1-MMP, which are involved in cancer progression.
Subunit:
Interacts with MMP-9.
Subcellular Location:
Cell membrane; Lipid-anchor, GPI-anchor.
Tissue Specificity:
Expressed in various tissues and untransformed cells. It is undetectable in tumor-derived cell lines and oncogenically transformed cells.
Post-translational modifications:
N-glycosylated.