JMY
JMY (junction mediating and regulatory protein, p53 cofactor; also known as FLJ37870 and WHAMM2) is a dual-function protein that acts as a nuclear p53 cofactor and a cytoplasmic regulator of actin dynamics. Its activity depends on where it sits in the cell. Browse Assay Genie's current range of JMY research reagents below, or read on for the biology behind the target.
JMY acts both as a nuclear p53 (TP53) cofactor and as a cytoplasmic regulator of actin dynamics, and the two activities are regulated by its subcellular location. In the nucleus it increases the p53 response through its interaction with p300 (EP300). It enhances p53-dependent transcription and apoptosis, which points to a role in p53-mediated stress responses such as DNA damage.
In the cytoplasm, JMY is a nucleation-promoting factor for both branched and unbranched actin filaments. It activates the Arp2/3 complex to build branched actin networks. It can also catalyse actin polymerisation without Arp2/3, producing unbranched filaments. One proposed model is that JMY first nucleates new mother filaments and then activates Arp2/3 to branch off them, allowing a branched network to form rapidly. Through this control of actin dynamics, JMY contributes to cell motility. On nutrient stress, MAP1LC3B recruits JMY directly to phagophore membrane surfaces, where it promotes actin assembly during autophagy.
The human JMY gene encodes a member of the JMY family, and HGNC places it in the Wiskott-Aldrich Syndrome protein family. UniProt lists localisation to the nucleus, cytoplasmic vesicles, the cytoskeleton, the endomembrane system and the autophagosome membrane. NCBI Gene also notes microtubule binding activity, a role in the cellular response to starvation, and localisation to the cell leading edge. The mouse ortholog is Jmy. Researchers studying p53 signalling, actin remodelling or autophagy use JMY as a protein that links these processes.
JMY increases p53-dependent transcription and apoptosis through p300, making it relevant to studies of DNA damage signalling.
JMY nucleates branched and unbranched filaments and activates the Arp2/3 complex, so it is used to study actin assembly.
JMY controls actin dynamics and localises to the cell leading edge, linking it to the cytoskeletal basis of cell movement.
MAP1LC3B recruits JMY to phagophore membranes on nutrient stress, where it promotes actin assembly during autophagy.
JMY has two roles depending on its location. In the nucleus it is a p53 cofactor that works with p300 to enhance p53-dependent transcription and apoptosis. In the cytoplasm it promotes actin nucleation, activating Arp2/3 and also forming unbranched filaments, and it supports autophagy.
JMY stands for junction mediating and regulatory protein, p53 cofactor. UniProt calls it junction-mediating and -regulatory protein. Aliases include FLJ37870 and WHAMM2, and HGNC lists it in the Wiskott-Aldrich Syndrome protein family. Check the datasheet of any product for its validated reactivity.
A mouse ortholog, Jmy, is recorded for the human gene. No rat ortholog is given in the data used here. The dual nuclear and cytoplasmic functions described for JMY come from UniProt annotation. Check the datasheet of any product for its validated reactivity.
Other WASP family members, p53 pathway proteins and autophagy markers with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt Q8N9B5; product specifications from Assay Genie datasheets.