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COL27A1 Knockout Cell Lines

Gene: COL27A1

Official Full Name: collagen type XXVII alpha 1 chainprovided by HGNC

Gene Summary: This gene encodes a member of the fibrillar collagen family, and plays a role during the calcification of cartilage and the transition of cartilage to bone. The encoded protein product is a preproprotein. It includes an N-terminal signal peptide, which is followed by an N-terminal propetide, mature peptide and a C-terminal propeptide. The N-terminal propeptide contains thrombospondin N-terminal-like and laminin G-like domains. The mature peptide is a major triple-helical region. The C-terminal propeptide, also known as COLFI domain, plays crucial roles in tissue growth and repair. Mutations in this gene cause Steel syndrome. Alternatively spliced transcript variants have been found, but the full-length nature of some variants has not been determined. [provided by RefSeq, Sep 2014]

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Products Background

Products

Catalog Number Product Name Species Gene Passage ratio Mycoplasma testing Price
KO24307 COL27A1 Knockout cell line (HeLa) Human COL27A1 1:3~1:6 Negative Online Inquiry
KO24308 COL27A1 Knockout cell line (HCT 116) Human COL27A1 1:2~1:4 Negative Online Inquiry
KO24309 COL27A1 Knockout cell line (HEK293) Human COL27A1 1:3~1:6 Negative Online Inquiry
KO24310 COL27A1 Knockout cell line (A549) Human COL27A1 1:3~1:4 Negative Online Inquiry

Background

COL27A1 Gene Knockout Cell Lines are genetically engineered cell lines specifically designed to lack the expression of the COL27A1 (Collagen Type XXVII Alpha 1) gene. These cell lines serve as crucial tools for studying the functional impacts of COL27A1 deficiency, which is essential for understanding various pathological conditions, including certain types of skeletal disorders and cancers. By providing a controlled environment to observe the absence of this collagen subtype, researchers can dissect the biological pathways affected by COL27A1 and explore its roles in cellular processes such as tissue regeneration, extracellular matrix formation, and cell signaling.

The mechanisms underlying the utility of COL27A1 Knockout Cell Lines involve the use of advanced CRISPR-Cas9 technology or other gene-editing techniques, which ensure precise knockout of the target gene. This targeted approach not only allows for accurate modeling of disease conditions but also enables researchers to monitor alterations in cellular characteristics, including proliferation, differentiation, and apoptosis. Such insights are critical in elucidating the biological significance of COL27A1 and its potential involvement in therapeutic interventions.

The scientific importance of these cell lines extends into both research and clinical applications. In research settings, they facilitate the investigation of COL27A1's role in mechanobiology and cellular response to environmental stimuli. Clinically, understanding the pathways affected by COL27A1 knockouts could pave the way for innovations in drug development and regenerative medicine, potentially leading to targeted therapies for conditions related to collagen deficiencies.

Compared to conventional cell lines that express COL27A1, these knockout lines offer significant advantages, including the ability to systematically analyze the loss-of-function effects without interference from compensatory gene expressions. This specificity in functional studies could lead researchers to more definitive conclusions about the role of COL27A1 in health and disease.

In conclusion, COL27A1 Gene Knockout Cell Lines present a valuable resource for researchers and clinicians alike. Their precision and applicability in understanding complex biological systems underscore their importance in advancing scientific knowledge and therapeutic development. Our company, with years of expertise in producing high-quality genetic models, is committed to providing reliable and innovative biological products to meet the evolving needs of the scientific community.

Please note that all services are for research use only. Not intended for any clinical use.

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