Collagenase/Hyaluronidase

10X Collagenase/hyaluronidase in DMEM

Collagenase/Hyaluronidase

10X Collagenase/hyaluronidase in DMEM

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10X Collagenase/hyaluronidase in DMEM
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Product Advantages


  • Effectively dissociate human mammary tissue and prostate epithelial cells


Overview

Enzymatically dissociate human mammary cells with 10X Collagenase/Hyaluronidase in Dulbecco’s Modified Eagle’s Medium (DMEM). This protease/polysaccharidase combination digests native collagen fibrils and hydrolizes hyaluronic acids in connective tissues for effective tissue dissociation. Collagenase/Hyluronidase can also been used for enzymatic dissociation of prostate epithelial cells.
Contains
• 3000 U/mL Collagenase
• 1000 U/mL Hyaluronidase
• DMEM (1000 mg D-glucose/L)
Subtype
Enzymatic
Cell Type
Mammary Cells, Other, Prostate Cells
Species
Human, Mouse, Non-Human Primate, Other, Rat
Application
Cell Culture
Area of Interest
Epithelial Cell Biology

Protocols and Documentation

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

Document Type
Product Name
Catalog #
Lot #
Language
Catalog #
07912
Lot #
All
Language
English
Document Type
Safety Data Sheet
Catalog #
07912
Lot #
All
Language
English

Applications

This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.

Resources and Publications

Publications (2)

Silica bioreplication preserves three-dimensional spheroid structures of human pluripotent stem cells and HepG2 cells. Lou Y-R et al. Scientific reports 2015 SEP

Abstract

Three-dimensional (3D) cell cultures produce more in vivo-like multicellular structures such as spheroids that cannot be obtained in two-dimensional (2D) cell cultures. Thus, they are increasingly employed as models for cancer and drug research, as well as tissue engineering. It has proven challenging to stabilize spheroid architectures for detailed morphological examination. Here we overcome this issue using a silica bioreplication (SBR) process employed on spheroids formed from human pluripotent stem cells (hPSCs) and hepatocellular carcinoma HepG2 cells cultured in the nanofibrillar cellulose (NFC) hydrogel. The cells in the spheroids are more round and tightly interacting with each other than those in 2D cultures, and they develop microvilli-like structures on the cell membranes as seen in 2D cultures. Furthermore, SBR preserves extracellular matrix-like materials and cellular proteins. These findings provide the first evidence of intact hPSC spheroid architectures and similar fine structures to 2D-cultured cells, providing a pathway to enable our understanding of morphogenesis in 3D cultures.
Activation of the aryl hydrocarbon receptor AhR Promotes retinoic acid-induced differentiation of myeloblastic leukemia cells by restricting expression of the stem cell transcription factor Oct4. Bunaciu RP and Yen A Cancer research 2011 MAR

Abstract

Retinoic acid (RA) is used to treat leukemia and other cancers through its ability to promote cancer cell differentiation. Strategies to enhance the anticancer effects of RA could deepen and broaden its beneficial therapeutic applications. In this study, we describe a receptor cross-talk system that addresses this issue. RA effects are mediated by RAR/RXR receptors that we show are modified by interactions with the aryl hydrocarbon receptor (AhR), a protein functioning both as a transcription factor and a ligand-dependent adaptor in an ubiquitin ligase complex. RAR/RXR and AhR pathways cross-talk at the levels of ligand-receptor and also receptor-promoter interactions. Here, we assessed the role of AhR during RA-induced differentiation and a hypothesized convergence at Oct4, a transcription factor believed to maintain stem cell characteristics. RA upregulated AhR and downregulated Oct4 during differentiation of HL-60 promyelocytic leukemia cells. AhR overexpression in stable transfectants downregulated Oct4 and also decreased ALDH1 activity, another stem cell-associated factor, enhancing RA-induced differentiation as indicated by cell differentiation markers associated with early (CD38 and CD11b) and late (neutrophilic respiratory burst) responses. AhR overexpression also increased levels of activated Raf1, which is known to help propel RA-induced differentiation. RNA interference-mediated knockdown of Oct4 enhanced RA-induced differentiation and G(0) cell-cycle arrest relative to parental cells. Consistent with the hypothesized importance of Oct4 downregulation for differentiation, parental cells rendered resistant to RA by biweekly high RA exposure displayed elevated Oct4 levels that failed to be downregulated. Together, our results suggested that therapeutic effects of RA-induced leukemia differentiation depend on AhR and its ability to downregulate the stem cell factor Oct4.