Reversion-Inducing-Cysteine-Rich Protein with Kazal Motifs (RECK) (AA 559-760) antibody

Details for Product No. ABIN968568
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Synonyms ST15, St15, mRECK
AA 559-760
(15), (15), (6), (3), (3), (2), (1), (1), (1), (1)
(56), (22), (14)
(51), (6)
Clonality (Clone)
Monoclonal ()
(3), (3), (3), (2), (2), (2), (1), (1), (1), (1), (1), (1), (1), (1)
Western Blotting (WB), Immunofluorescence (IF)
(43), (21), (19), (18), (10), (10), (6), (5), (4), (3), (2), (1), (1)
Pubmed 3 references available
Quantity 50 μg
Shipping to United States (Change)
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Catalog No. ABIN968568
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Immunogen Human RECK
Clone MOC-31
Isotype IgG1
Characteristics 1. Since applications vary, each investigator should titrate the reagent to obtain optimal results.
2. Please refer to us for technical protocols.
3. Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.
4. Source of all serum proteins is from USDA inspected abattoirs located in the United States.
Purification Purified from tissue culture supernatant or ascites by affinity chromatography.
Alternative Name RECK
Background Reversion-inducing-cysteine-rich protein with Kazal motifs (RECK) was identified in an assay that characterized genes inducing flat morphology in a v-Ki-ras-transformed NIH 3T3 cell line. RECK is a glycoprotein that contains two hydrophobic regions, the C-terminal is involved in GPI-anchoring, five repeats of a putative six-cysteine knot motif, two EGF-like regions (E), and three serine-protease inhibitor-like domains (S), one of which (635-654) is a Kazal motif (C-X7-C-X6-Y-X3-C-X2.3-C). In normal human tissues, RECK is expressed ubiquitously, however it is not detectable in many malignant cell lines. Downregulation of RECK transcription in malignant cells may involve ras-dependent negative regulation of the RECK gene via an upstream promoter region that contains an Sp1 motif. Transfection of tumor cell lines with RECK can inhibit tumor invasion and metastatic activity independent of chemotactic activity. This inhibitory effect may be a result RECK-induced inhibition of MMP-9 secretion or protease activity. Thus, RECK may be an important inhibitor of matrix metalloproteinase activity and suppression of RECK may be required for both tumor cell invasion and metastasis.
Synonyms: Reversion-inducing-cysteine-rich protein with Kazal motifs
Molecular Weight 110 kDa
Research Area Proteolysis / Ubiquitin

Related Products: ABIN968553, ABIN967389

Restrictions For Research Use only
Format Liquid
Concentration 250 µg/ml
Buffer Aqueous buffered solution containing BSA, glycerol.
Preservative Sodium azide
Precaution of Use This product contains sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Storage -20 °C
Supplier Images
anti-Reversion-Inducing-Cysteine-Rich Protein with Kazal Motifs (RECK) (AA 559-760) antibody Immunofluorescence staining of HeLa cells (Human cervical epitheloid carcinoma, ATCC CCL-2.2).
anti-Reversion-Inducing-Cysteine-Rich Protein with Kazal Motifs (RECK) (AA 559-760) antibody (2) Western blot analysis of RECK on a WI-38 cell lysate (Human lung fibroblasts, ATCC CCL-75). Lane 1: 1:250, lane 2: 1:500, lane 3: 1:1000 dilution of the mouse anti-human RECK antibody.
Product cited in: Sasahara, Takahashi, Noda: "Involvement of the Sp1 site in ras-mediated downregulation of the RECK metastasis suppressor gene." in: Biochemical and biophysical research communications, Vol. 264, Issue 3, pp. 668-75, 1999 (PubMed).

Sasahara, Takahashi, Sogayar et al.: "Oncogene-mediated downregulation of RECK, a novel transformation suppressor gene." in: Brazilian journal of medical and biological research = Revista brasileira de pesquisas médicas e biológicas / Sociedade Brasileira de Biofísica ... [et al.], Vol. 32, Issue 7, pp. 891-5, 1999 (PubMed).

Takahashi, Sheng, Horan et al.: "Regulation of matrix metalloproteinase-9 and inhibition of tumor invasion by the membrane-anchored glycoprotein RECK." in: Proceedings of the National Academy of Sciences of the United States of America, Vol. 95, Issue 22, pp. 13221-6, 1998 (PubMed).

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