Gene: CAPN10
Official Full Name: calpain 10provided by HGNC
Gene Summary: Calpains represent a ubiquitous, well-conserved family of calcium-dependent cysteine proteases. The calpain proteins are heterodimers consisting of an invariant small subunit and variable large subunits. The large catalytic subunit has four domains: domain I, the N-terminal regulatory domain that is processed upon calpain activation; domain II, the protease domain; domain III, a linker domain of unknown function; and domain IV, the calmodulin-like calcium-binding domain. This gene encodes a large subunit. It is an atypical calpain in that it lacks the calmodulin-like calcium-binding domain and instead has a divergent C-terminal domain. It is similar in organization to calpains 5 and 6. This gene is associated with type 2 or non-insulin-dependent diabetes mellitus (NIDDM), and is located within the NIDDM1 region. Multiple alternative transcript variants have been described for this gene. [provided by RefSeq, Sep 2010]
Catalog Number | Product Name | Species | Gene | Passage ratio | Mycoplasma testing | Price |
---|---|---|---|---|---|---|
KO31177 | CAPN10 Knockout cell line (HeLa) | Human | CAPN10 | 1:3~1:6 | Negative | Online Inquiry |
KO31178 | CAPN10 Knockout cell line (HCT 116) | Human | CAPN10 | 1:2~1:4 | Negative | Online Inquiry |
KO31179 | CAPN10 Knockout cell line (HEK293) | Human | CAPN10 | 1:3~1:6 | Negative | Online Inquiry |
KO31180 | CAPN10 Knockout cell line (A549) | Human | CAPN10 | 1:3~1:4 | Negative | Online Inquiry |
CAPN10 Gene Knockout Cell Lines are specialized cellular models that have undergone targeted gene deletion of the CAPN10 gene, which encodes the calcium-dependent cysteine protease calpain-10. These cell lines are invaluable for studying the role of CAPN10 in cellular processes, particularly in the context of insulin signaling, metabolism, and related pathophysiologies such as type 2 diabetes. By eliminating the CAPN10 gene, researchers can directly observe the effects of its absence on cell physiology, molecular pathways, and overall metabolic function.
The primary mechanisms through which CAPN10 operates involve the regulation of intracellular calcium levels and the modulation of various signaling pathways. Its role in proteolytic processing is critical for maintaining cellular homeostasis, and the knockout of CAPN10 can help elucidate its contribution to metabolic disorders by allowing researchers to examine changes in insulin receptor signaling, glucose uptake, and lipid metabolism.
In scientific research, CAPN10 Gene Knockout Cell Lines have significant applications, particularly in diabetes studies, pharmacological screening, and cellular metabolism investigations. They provide a robust platform for understanding the underlying mechanisms that lead to insulin resistance and other metabolic dysregulations, which are essential for developing novel pharmaceutical interventions.
What sets these cell lines apart from alternative models is their specificity and the precision of the knockout, which enhances the validity of experimental outcomes. With high reproducibility and availability of characterized lines, researchers can have confidence in deriving meaningful conclusions from their experiments.
For researchers and clinicians focused on metabolic diseases, understanding CAPN10's role in cellular function offers the potential to identify novel therapeutic targets and enhance treatment strategies. Consequently, CAPN10 Gene Knockout Cell Lines represent a powerful tool for driving innovative research in diabetes and metabolic regulation.
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