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MRPS11 Knockout Cell Lines

Gene: MRPS11

Official Full Name: mitochondrial ribosomal protein S11provided by HGNC

Gene Summary: Mammalian mitochondrial ribosomal proteins are encoded by nuclear genes and help in protein synthesis within the mitochondrion. Mitochondrial ribosomes (mitoribosomes) consist of a small 28S subunit and a large 39S subunit. They have an estimated 75% protein to rRNA composition compared to prokaryotic ribosomes, where this ratio is reversed. Another difference between mammalian mitoribosomes and prokaryotic ribosomes is that the latter contain a 5S rRNA. Among different species, the proteins comprising the mitoribosome differ greatly in sequence, and sometimes in biochemical properties, which prevents easy recognition by sequence homology. This gene encodes a 28S subunit protein that contains a high level of sequence similarity with ribosomal protein S11P family members. A pseudogene corresponding to this gene is found on chromosome 20. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Apr 2016]

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Products Background

Products

Catalog Number Product Name Species Gene Passage ratio Mycoplasma testing Price
KO16040 MRPS11 Knockout cell line (HeLa) Human MRPS11 1:3~1:6 Negative Online Inquiry
KO16041 MRPS11 Knockout cell line (HCT 116) Human MRPS11 1:2~1:4 Negative Online Inquiry
KO16042 MRPS11 Knockout cell line (HEK293) Human MRPS11 1:3~1:6 Negative Online Inquiry

Background

MRPS11 Gene Knockout Cell Lines are genetically engineered cell lines specifically designed to study the implications of the MRPS11 gene, which encodes a mitochondrial ribosomal protein integral to mitochondrial protein synthesis and cellular bioenergetics. These knockout cell lines provide researchers with a potent tool for investigating the functional consequences of MRPS11 deficiency, enabling comprehensive insights into mitochondrial dysfunction, metabolic disorders, and their potential linkage to various pathologies.

The MRPS11 knockout mechanism involves targeted gene disruption via CRISPR-Cas9 technology or similar gene-editing approaches, effectively abolishing the expression of the MRPS11 protein. This disruption alters mitochondrial translation processes, leading to a cascade of physiological changes that researchers can analyze. By studying these alterations, scientists can elucidate the role of MRPS11 in mitochondrial homeostasis and its broader implications in diseases associated with cellular energy metabolism.

The scientific importance of MRPS11 Gene Knockout Cell Lines extends to both fundamental research and clinical applications. In basic research, these cell lines serve as a model to dissect mitochondrial biology, investigate the molecular mechanisms underlying metabolic syndromes, and explore potential therapeutic targets. Clinically, understanding the role of MRPS11 in disease can inform the development of novel treatments and strategies for managing mitochondrial diseases, an area that continues to be a significant challenge in modern medicine.

What sets MRPS11 Gene Knockout Cell Lines apart from conventional cell lines is their specificity and reliability. These cell lines allow for targeted studies regarding mitochondrial function without the interference of baseline MRPS11 activity, thus providing unambiguous results that can be replicated. Moreover, given the increasing incidence of mitochondrial diseases, researchers and clinicians can utilize these models to forge new pathways in understanding and treating patient conditions.

Ultimately, MRPS11 Gene Knockout Cell Lines represent a critical asset for researchers, offering clear advantages in precision and applicability in both experimental and clinical settings. With our company’s solid expertise in developing high-quality genetic models and commitment to supporting scientific inquiry, we strive to empower breakthroughs in mitochondrial research and therapy with our innovative product offerings.

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

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