Description
Key facts
Cell type:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 1 bp deletion in exon 2 and 1 bp insertion in exon 2 and 4 bp deletion in exon 2
Product details:
We will provide viable cells that proliferate on revival.
This product is subject to limited use licenses from The Broad Institute, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our
limited use license
patent pages
Properties and Storage Information:
Gene name-GHITM, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--196°C, Appropriate long-term storage conditions--196°C
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
MICS1 also known as mitochondrial import inner membrane translocase subunit 13 is a protein that plays a role in the transport of polypeptides across the mitochondrial inner membrane. It has an approximate mass of 13 kDa. You can find MICS1 expression predominantly in tissues with high-energy demands such as muscle and brain tissues where efficient mitochondrial function is critical.
Biological function summary
MICS1 contributes to the establishment of the mitochondrial inner membrane potential essential for maintaining proper mitochondrial function. MICS1 forms part of the translocase of inner membrane (TIM) complex which facilitates the import of preproteins into the mitochondria. This activity supports cellular energy metabolism by ensuring efficient electron transport chain operation and ATP production.
Pathways
MICS1 is involved in the mitochondrial protein import pathway and the maintenance of mitochondrial membrane potential. It interacts with other components of the TIM complex such as Tim23 and works closely with proteins in the oxidative phosphorylation pathway. These interactions ensure a seamless integration of imported mitochondrial proteins into the inner membrane facilitating cellular energy production processes.
MICS1 has links to conditions related to mitochondrial dysfunction such as mitochondrial myopathy and Leigh syndrome. Dysregulation of MICS1 may disrupt mitochondrial protein import and membrane potential maintenance contributing to these conditions. Its interaction with other mitochondrial proteins like Tim23 further associates it with the broader mitochondrial dysfunction often present in these diseases.
