Human Cystatin SN/CST1 ELISA Kit (DEIABL612)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
96T
Sample
cell culture supernates, serum, heparin plasma, EDTA plasma, saliva, urine
Species Reactivity
Human
Intended Use
Sandwich High Sensitivity ELISA kit for Quantitative Detection of Human Cystatin SN/CST1.
Storage
Store at 4°C for 6 months, at -20°C for 12 months. Avoid multiple freeze-thaw cycles(Shipped with wet ice.)
Detection Range
156pg/ml-10000pg/ml
Sensitivity
<10pg/ml

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References


CAPC negatively regulates NF-kappa B activation and suppresses tumor growth and metastasis

ONCOGENE

Authors: Liu, X-F; Xiang, L.; Zhang, Y.; Becker, K. G.; Bera, T. K.; Pastan, I.

CAPC, also known as LRRC26, is expressed in normal prostate and salivary gland. We developed a mAb to CAPC and used it to characterize the protein and study its function. CAPC protein was detected in normal prostate and salivary gland, in several human breast cancer cell lines and in the prostate cancer cell line LNCaP. Knockdown of CAPC by siRNA in LNCaP cells enhanced anchorage-independent growth in soft agar. Conversely, overexpression of CAPC in MDA-231 breast cancer cells and A431 epidermoid cancer cells inhibited growth in soft agar and tumorigenesis in nude mice, and suppressed the metastasis of MDA-231 cells to the lung. Overexpression of CAPC downregulated NF-kappa B activity and its target genes, including GM-CSF (CSF2), CXCL1, IL8 and LTB1. It also suppressed genes encoding the serine protease mesotrypsin (PRSS3) and cystatin SN (CST1). CAPC expressing tumors showed a decrease in the number of proliferating cells and a large increase in ECM. The role of CAPC in the suppression of tumor growth and metastasis may be through its alteration of the tumor microenvironment. Oncogene (2012) 31, 1673-1682; doi:10.1038/onc.2011.355; published online 8 August 2011

Transcriptome analysis of a human colorectal cancer cell line shows molecular targets of insulin-like growth factor-binding protein-4 overexpression

INTERNATIONAL JOURNAL OF CANCER

Authors: Diehl, D; Lahm, H; Wolf, E; Bauersachs, S

Insulin-like growth factor II (IGF-II) is expressed commonly in colorectal tumors. IGF-binding protein-4 (IGFBP-4) counteracts the tumor promoting activities of IGF-II by binding this growth factor. We have shown previously that in LS1034 cells, which highly express IGF-II, overexpression of IGFBP-4 led to a strong reduction in proliferation, colony formation and invasive capacity. To investigate the effects of IGFBP-4 at the molecular level we analyzed growth parameters of LS1034 human colon cancer cells vs. cells expressing the murine IGFBP-4 (mIGFBP-4) and used a subtractive cDNA library approach in combination with cDNA array hybridization to detect changes in the mRNA expression profiles. The mRNA levels for several proteins that are known to affect important biological properties of neoplastic cells, such as proteolysis' proliferation and differentiation were altered by overexpression of IGFBP-4. Transcript levels for tumor markers, like the carcinoembryonic antigen-related cell adhesion molecule (CEACAM), were reduced by elevated mIGFBP-4. Changes at the mRNA level were confirmed by Western blotting for CST1 (proteolysis or protease inhibitor), COX-2 (cell motility) and CEACAM5 (tumor marker). Furthermore, the effect of mIGFBP-4 on apoptosis was investigated and no increase of apoptosis could be detected in the IGFBP-4 overexpressing LS1034 cells. Our data indicate that IGFBP-4 is involved in the regulation of gene products that are known or supposed to be important for the pathogenesis of colon cancer cells. (C) 2004 Wiley-Liss, Inc.

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