CTTN
CTTN (cortactin, also known as EMS1) is a Src substrate that helps organise the actin cytoskeleton and cell shape. It contributes to lamellipodia formation, cell migration, adhesion and endocytosis, and is linked to cancer cell invasiveness. Browse Assay Genie's current range of CTTN research reagents below, or read on for the biology behind the target.
CTTN, or cortactin, contributes to the organisation of the actin cytoskeleton and to cell shape. It plays a role in the formation of lamellipodia and in cell migration, and in focal adhesion assembly and turnover. In complex with ABL1 and MYLK, it regulates the cortical actin-based cytoskeletal rearrangement that is critical for sphingosine 1-phosphate (S1P)-mediated enhancement of the endothelial cell barrier.
Beyond the cytoskeleton, cortactin takes part in intracellular protein transport and endocytosis, including receptor-mediated endocytosis via clathrin-coated pits. It also modulates the levels of potassium channels at the cell membrane and is required for stabilisation of KCNH1 channels there. In neurons it regulates morphology, axon growth and the formation of growth cones, and through its interaction with CTTNBP2 it is involved in the regulation of neuronal spine density. UniProt records localisation to the cytoskeleton, lamellipodia, ruffles, podosomes, focal adhesions, dendritic spines, the cell cortex and the endoplasmic reticulum. The mouse and rat orthologues are both named Cttn.
The CTTN gene is classed by HGNC in the SH3 domain containing group. Its previous name, ems1, refers to the mammary tumour and squamous cell carcinoma-associated p80/85 Src substrate. NCBI Gene reports that the gene is overexpressed in breast cancer and in squamous cell carcinomas of the head and neck, and that the protein regulates interactions between components of adherens-type junctions and organises the cytoskeleton and adhesion structures of epithelia and carcinoma cells. During apoptosis the protein is degraded in a caspase-dependent manner. Aberrant regulation contributes to tumour cell invasion and metastasis, and three splice variants encoding different isoforms have been identified.
Cortactin is linked to the invasiveness of cancer cells and the formation of metastases, and is overexpressed in breast and head and neck squamous cell carcinomas.
CTTN contributes to lamellipodia formation and actin organisation, making it a relevant target for studies of cell motility and shape.
With ABL1 and MYLK, cortactin regulates cortical actin rearrangement underlying S1P-mediated enhancement of the endothelial cell barrier.
Cortactin influences axon growth, growth cone formation and, with CTTNBP2, neuronal spine density.
CTTN (cortactin) helps organise the actin cytoskeleton and cell shape. It contributes to lamellipodia formation, cell migration, focal adhesion turnover, endocytosis via clathrin-coated pits and the stabilisation of potassium channels such as KCNH1 at the cell membrane. It also functions in neuronal morphology and spine density.
Cortactin is also known as EMS1, and UniProt names it Src substrate cortactin. The earlier gene name refers to the mammary tumour and squamous cell carcinoma-associated p80/85 Src substrate. NCBI Gene reports three splice variants encoding different isoforms.
NCBI Gene reports that CTTN is overexpressed in breast cancer and head and neck squamous cell carcinomas, and that aberrant regulation contributes to tumour cell invasion and metastasis. Orthologues named Cttn exist in mouse and rat; check the datasheet of any product for its validated reactivity.
Other actin-cytoskeleton regulators, Src-pathway proteins and cancer invasion markers with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt Q14247; product specifications from Assay Genie datasheets.