Catalyzes the specific attachment of an amino acid to its cognate tRNA in a 2 step reaction: the amino acid (AA) is first activated by ATP to form AA-AMP and then transferred to the acceptor end of the tRNA. When secreted, acts as a signaling molecule that induces immune response through the activation of monocyte/macrophages. Catalyzes the synthesis of the signaling molecule diadenosine tetraphosphate (Ap4A), and thereby mediates disruption of the complex between HINT1 and MITF and the concomitant activation of MITF transcriptional activity. Interacts with HIV-1 virus GAG protein, facilitating the selective packaging of tRNA3(Lys), the primer for reverse transcription initiation.
This gene encodes a type I integral membrane glycoprotein.The encoded protein acts as a receptor and binds to both soluble and immobilized hyaluronan. This protein may function in lymphatic hyaluronan transport and have a role in tumor metastasis.
May be involved in transcriptional regulation through interaction with SNW1 and recruiting histone deactelyase HDAC1. May inhibit notch intracellular domain (NICD) transactivation. May play a role in embryonal development and tumor transformation or aspects of tumor progression. Antigen recognized on a melanoma by autologous cytolytic T-lymphocytes.
MAG (Myelin-associated glycoprotein) is a type I transmembrane glycoprotein expressed by Schwann cells and oligodendrocytes, that has been implicated in the control of axonal growth in many neuronal populations including cerebellar granule neurons (CGNs).
Protease that enhances BCL10-induced activation: acts via formation of CBM complexes that channel adaptive and innate immune signaling downstream of CARD domain-containing proteins (CARD9, CARD11 and CARD14) to activate NF-kappa-B and MAP kinase p38 pathways which stimulate expression of genes encoding pro-inflammatory cytokines and chemokines.
Monoamine oxidase A (MAO-A), a mitochondrial enzyme, catalyzes the degradation of monoamines. Studies show that increased expression of MAO-A promotes prostate cancer metastasis by activating the Shh-IL6-RANKL signaling network. In addition, MAO-A expression in adipose tissue macrophages is upregulated in aging, leading to the reduction of noradrenaline availability in adipose tissue. Decreased levels of noradrenaline contribute to the aging-related decline of catecholamine-induced lipolysis in adipocytes. Furthermore, sympathetic neuron–associated macrophages import and degrade norepinephrine via the transporter SLC6A2 and MAO-A, respectively, and thus contribute to obesity.
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