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Additional recommended knowledge
MLN64 is hypothesized to regulate cholesterol transport between the late endosome and cytoplasmic membranes. It has also been proposed to mediate StAR-independent steroidogenesis, such as in the human placenta.
Its C-terminus contains a StAR-related transfer domain (START) that is homologous to the steroidogenic acute regulatory protein (StAR). X-ray crystallography indicates that this domain forms a pocket that can bind cholesterol. Its N-terminus consists of a MENTAL (MLN64 N-terminal) domain similar to the protein MLN64 N-terminal homologue (MENTHO) with unclear function.
MLN64 is expressed in all tissues in the body at various levels. In the brain, MLN64 is detectable in many but not all cells. Many malignant tumors highly express MLN64 as a result of its gene being part of a Her2/erbB2-containing gene locus that is duplicated.
Loss of MLN64 has little effect in mice. At the cellular level, changes in MLN64 can disrupt trafficking of endosomes and cause accumulation of cholesterol in late endosomes.
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "MLN64". A list of authors is available in Wikipedia.|