FITC标记的金属蛋白酶抑制因子RECK抗体
2017-5-3
英文名称Anti-RECK/FITC
中文名称FITC标记的金属蛋白酶抑制因子RECK抗体
别 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.
规格100ug
说 明 书100ug
研究领域肿瘤 免疫学 信号转导 细胞凋亡 转录调节因子
抗体来源Rabbit
克隆类型Polyclonal
交叉反应
产品应用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 状Lyophilized or Liquid
浓 度2mg/1ml
免 疫 原KLH conjugated synthetic peptide derived from human RECK
亚 型IgG
纯化方法affinity purified by Protein A
储 存 液0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存条件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.
产品介绍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.
中文名称FITC标记的金属蛋白酶抑制因子RECK抗体
别 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.
详细介绍：
规格100ug
说 明 书100ug
研究领域肿瘤 免疫学 信号转导 细胞凋亡 转录调节因子
抗体来源Rabbit
克隆类型Polyclonal
交叉反应
产品应用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 状Lyophilized or Liquid
浓 度2mg/1ml
免 疫 原KLH conjugated synthetic peptide derived from human RECK
亚 型IgG
纯化方法affinity purified by Protein A
储 存 液0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存条件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.
相关资料：
产品介绍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.
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