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基質金屬蛋白酶9抗體
  • 產品貨號:
    BN42203R
  • 中文名稱:
    基質金屬蛋白酶9抗體
  • 英文名稱:
    Rabbit anti-MMP9 Polyclonal antibody
  • 品牌:
    Biorigin
  • 貨號

    產品規格

    售價

    備注

  • BN42203R-50ul

    50ul

    ¥1486.00

    交叉反應:Human,Dog(predicted:Mouse,Rat,Chicken,Pig,Horse,Rabbit,Sheep) 推薦應用:WB,IHC-P,IHC-F,IF,ELISA

  • BN42203R-100ul

    100ul

    ¥2360.00

    交叉反應:Human,Dog(predicted:Mouse,Rat,Chicken,Pig,Horse,Rabbit,Sheep) 推薦應用:WB,IHC-P,IHC-F,IF,ELISA

  • BN42203R-200ul

    200ul

    ¥3490.00

    交叉反應:Human,Dog(predicted:Mouse,Rat,Chicken,Pig,Horse,Rabbit,Sheep) 推薦應用:WB,IHC-P,IHC-F,IF,ELISA

產品描述

英文名稱MMP9
中文名稱基質金屬蛋白酶9抗體
別    名Matrix metalloproteinase-9 precursor; MMP-9; MMP9; MMP 9; 92 kDa type IV; Collagenase; 92 kDa gelatinase; Gelatinase B; GELB; MMP9_HUMAN; 82 kDa matrix metalloproteinase-9; 92 kDa type IV collagenase; CLG 4B; CLG-4B; CLG4B; Collagenase Type 4 beta; Collagenase Type-4 beta; Collagenase type IV 92 KD; Collagenase type IV 92 KD; EC 3.4.24.35; Gelatinase 92 KD; Gelatinase 92 KD; Gelatinase beta; Gelatinase-beta; GelatinaseB; GELB; Macrophage gelatinase; MANDP2; Matrix metallopeptidase 9 (gelatinase B, 92kDa gelatinase, 92kDa type IV collagenase); Matrix Metalloproteinase 9; Type V collagenase.  





研究領域腫瘤  細胞生物  免疫學  神經生物學  信號轉導  轉錄調節因子  合成與降解  
抗體來源Rabbit
克隆類型Polyclonal
交叉反應Human, Dog,  (predicted: Mouse, Rat, Chicken, Pig, Horse, Rabbit, Sheep, )
產品應用WB=1:500-2000 ELISA=1:5000-10000 IHC-P=1:100-500 IHC-F=1:100-500 IF=1:100-500 (石蠟切片需做抗原修復)
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量78kDa
細胞定位細胞外基質 分泌型蛋白 
性    狀Liquid
濃    度1mg/ml
免 疫 原KLH conjugated synthetic peptide derived from human MMP9:151-250/707 
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Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
PubMedPubMed
產品介紹All cells within tissues are surrounded by an extracellular matrix (ECM) giving the tissues shape and structure. The ECM is constantly being remodeled and constant communication is maintained between cells through this matrix. Secreted proteins, termed matrix metalloproteinases (MMPs), are involved in the modulation of cell matrix interactions. MMPs are Zn(2+) binding endopeptidases that degrade various components of the ECM. MMPs are enzymes implicated in normal and pathologic tissue remodeling processes, wound healing, angiogenesis, and tumor invasion. These enzymes are very potent when active, and are associated with extracellular space inhibitors called TIMPs (tissue inhibitors of matrix metalloproteinases). TIMPs have been shown to block tumor cell invasion suggesting that they act as metastasis suppressor genes.

Function:
May play an essential role in local proteolysis of the extracellular matrix and in leukocyte migration. Could play a role in bone osteoclastic resorption. Cleaves KiSS1 at a Gly-|-Leu bond. Cleaves type IV and type V collagen into large C-terminal three quarter fragments and shorter N-terminal one quarter fragments. Degrades fibronectin but not laminin or Pz-peptide.

Subunit:
Exists as monomer or homodimer; disulfide-linked. Exists also as heterodimer with a 25 kDa protein. Macrophages and transformed cell lines produce only the monomeric form. Interacts with ECM1.

Subcellular Location:
Secreted, extracellular space, extracellular

Tissue Specificity:
Produced by normal alveolar macrophages and granulocytes.

Post-translational modifications:
Processing of the precursor yields different active forms of 64, 67 and 82 kDa. Sequentially processing by MMP3 yields the 82 kDa matrix metalloproteinase-9.
N- and O-glycosylated.

DISEASE:
Defects in MMP9 may be a cause of susceptibility to intervertebral disc disease (IDD) [MIM:603932]; also known as lumbar disk herniation (LDH). IDD is one of the most common musculo-skeletal disorders and the predominant cause of low-back pain and unilateral leg pain.
Defects in MMP9 are the cause of metaphyseal anadysplasia type 2 (MANDP2) [MIM:613073]. Metaphyseal anadysplasia consists of an abnormal bone development characterized by severe skeletal changes that, in contrast with the progressive course of most other skeletal dysplasias, resolve spontaneously with age. Clinical characteristics are evident from the first months of life and include slight shortness of stature and a mild varus deformity of the legs. Patients attain a normal stature in adolescence and show improvement or complete resolution of varus deformity of the legs and rhizomelic micromelia.

Similarity:
Belongs to the peptidase M10A family.

SWISS:
P14780

Gene ID:
4318

Database links:

Entrez Gene: 403885 Dog

Entrez Gene: 4318 Human

Entrez Gene: 17395 Mouse

Entrez Gene: 81687 Rat

Omim: 120361 Human

SwissProt: O18733 Dog

SwissProt: P14780 Human

SwissProt: P41245 Mouse

SwissProt: P50282 Rat

Unigene: 297413 Human

Unigene: 4406 Mouse

Unigene: 10209 Rat




Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

MMP9亦稱IV型膠原酶或明膠酶B,其主要功能為降解IV型膠原。因而它在腫瘤細胞突破基底膜屏障和浸潤轉移中起重要作用。目前主要用于各種惡性腫瘤(如乳腺癌、胃腸道癌、卵巢癌、膀胱癌等)中的基底膜檢測與轉移浸潤的研究。細胞外基質在維持正常組織結構與功能以及細胞生長和分化過程中起重要作用。細胞外基質動態平衡的失調與腫瘤細胞侵襲、轉移和復發密切相關,基質金屬蛋白酶(MMP9)是細胞外基質的降解酶,可降解Ⅳ、Ⅴ、Ⅸ、Ⅺ型膠原,在腫瘤的浸潤、轉移過程中起重要作用,近年為腫瘤研究的熱點。
鹽酸強力霉素還是多種基質金屬蛋白酶(MMPs)的抑制劑,包括MMP-8(neutrophil collagenase; IC50 =30 μM)和MMP-1(interstitial collagenase; IC50 = 300 μM)。研究報道,復發性角膜糜爛研究中它能夠顯著降低MMP-9的表達水平和活性。