GHITM
GHITM (growth hormone inducible transmembrane protein) is a mitochondrial inner membrane protein that maintains mitochondrial morphology and mediates calcium and potassium/proton exchange. It is also known as TMBIM5, MICS1, HSPC282, PTD010, DERP2 and My021. Browse Assay Genie's current range of GHITM research reagents below, or read on for the biology behind the target.
GHITM plays an important role in maintaining mitochondrial morphology and in mediating either calcium or potassium/proton antiport. It mediates proton-dependent calcium efflux from the mitochondrion and also functions as an electroneutral mitochondrial proton/potassium exchanger. The protein is required for the mitochondrial tubular network and for cristae organisation, and it is involved in the apoptotic release of cytochrome c. NCBI Gene annotation likewise describes calcium:proton antiporter activity, a role in calcium export from the mitochondrion, inner mitochondrial membrane organisation and negative regulation of cytochrome c release.
GHITM also acts as a regulator of mitochondrial proteostasis. It inhibits the proteolytic activity of AFG3L2, which stimulates respiration and stabilises respiratory enzymes in actively respiring mitochondria. When mitochondria become hyperpolarised, GHITM loses this inhibitory activity. The now active AFG3L2 turns first on GHITM and, if hyperpolarisation persists, on other mitochondrial proteins, leading to broad remodelling of the mitochondrial proteome.
The GHITM gene encodes a protein of the BI1 family, grouped by HGNC among the transmembrane BAX inhibitor motif containing genes, which accounts for the alias TMBIM5. The protein is located in the mitochondrial inner membrane, and the NCBI Gene summary also reports it in the endoplasmic reticulum membrane. Orthologues are annotated in mouse and rat, both named Ghitm. Researchers studying GHITM often work on mitochondrial ion homeostasis, cristae structure and the control of apoptosis.
GHITM mediates proton-dependent calcium efflux from mitochondria, making it relevant to studies of calcium export and ion homeostasis.
The protein is required for the mitochondrial tubular network and cristae organisation, supporting work on inner membrane architecture.
GHITM is involved in the apoptotic release of cytochrome c and negatively regulates its release from mitochondria.
GHITM inhibits AFG3L2 in respiring mitochondria, and this control is lost on hyperpolarisation, remodelling the mitochondrial proteome.
GHITM maintains mitochondrial morphology and cristae organisation. It mediates proton-dependent calcium efflux and acts as an electroneutral proton/potassium exchanger. It also inhibits the protease AFG3L2 in actively respiring mitochondria, which stimulates respiration and stabilises respiratory enzymes.
GHITM is also called TMBIM5 and MICS1, reflecting its place among the transmembrane BAX inhibitor motif containing genes. Other aliases are HSPC282, PTD010, DERP2 and My021. UniProt lists the protein name as growth hormone-inducible transmembrane protein.
Mouse and rat orthologues are both named Ghitm. GHITM belongs to the BI1 family and is involved in the apoptotic release of cytochrome c, with NCBI Gene noting negative regulation of cytochrome c release. Check the datasheet of any product for its validated reactivity.
Other BI1 family members, mitochondrial proteases and apoptosis-related proteins with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt Q9H3K2; product specifications from Assay Genie datasheets.