Anti-hnRNP M3-M4 antibody [2A6-2H3]

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

The heterogeneous nuclear ribonucleoprotein M (hnRNP M3-M4) is a member of the hnRNP family known to play a role in RNA binding and processing. Often referred to as hnRNP M it consists of multiple isoforms with a mass around 72 kDa. This protein expresses mainly in the nucleus of cells but it may also present in the cytoplasm under certain conditions. It contains RNA recognition motifs (RRMs) that allow it to bind various RNA substrates influencing the maturation and transport of mRNA.

Biological function summary

HnRNP M3-M4 influences mRNA splicing and gene expression. It potentially forms part of larger ribonucleoprotein complexes and contributes to the regulation of alternative splicing events. These splicing events play significant roles in generating protein diversity given they allow a single gene to encode multiple proteins. Consequently hnRNP M3-M4 holds an effect over cellular responses to developmental cues and environmental changes due to its involvement in expression regulation.

Pathways

HnRNP M3-M4 interacts with several splicing-related pathways. It participates in the alternative splicing pathway allowing cells to adapt to functional requirements by modulating protein products. The protein shows connections with other splicing factors like serine/arginine-rich splicing factor 1 (SRSF1) working to control splicing accuracy and efficiency. Another pathway where hnRNP M3-M4 might play a role is the mRNA transport pathway facilitating the movement from nucleus to cytoplasm.

Associated diseases and disorders

HnRNP M3-M4 connects to conditions such as cancer and neurodegenerative diseases. Abnormal splicing activities and expressions can lead to oncogenic transformation implicating hnRNP M3-M4 in various cancers. Moreover in neurodegenerative diseases it could interact with proteins like TAR DNA-binding protein 43 (TDP-43) associating with neurodegenerative processes. These interactions suggest that irregularities in hnRNP M3-M4 function or regulation can contribute to disease progression.