Disease relevance of CRSP3

• Melanoma metastasis suppression by chromosome 6: evidence for a pathway regulated by CRSP3 and TXNIP [1].
• Quantitative real-time reverse-transcription PCR of clinical melanoma samples showed that loss of CRSP3 expression correlated with decreased KISS1 expression and increased metastasis [1].
• Requirement of Sur2 for efficient replication of mouse adenovirus type 1 [2].

High impact information on CRSP3

• Active and repressive C/EBPbeta interacts with multisubunit Mediator complexes through the CRSP130/Sur2 subunit [3].
• Knockdown of CRSP130/Sur2 prevents Mediator binding and transactivation through C/EBPbeta [3].
• SUR1- and SUR2-based channels are distinguished by their differential sensitivity to sulfonylureas, whereas SUR2A-based channels are distinguished from SUR2B channels by their differential sensitivity to diazoxide [4].
• Quantitative immunoblotting indicated that there are about 3 x 10(5) to 6 x 10(5) molecules of hSur2 Mediator subunit per HeLa cell, i.e., the same order of magnitude as RNA polymerase II and general transcription factors [5].
• PCR karyotyping that refined the region on chromosome 6 identified CRSP3/DRIP130, a transcriptional coactivator, as a metastasis suppressor [1].

Chemical compound and disease context of CRSP3

• Although it has been proposed that human adenovirus E1A recruits the Mediator complex to transactivate transcription of viral early genes, Sur2 function in adenovirus replication has not been directly tested previously [2].

Biological context of CRSP3

• The viral replication defects in Sur2(-/-) MEFs appeared to be due at least in part to a defect in viral early gene transcription [2].
• In coinfection experiments, the ratio of sur2 colonies to wild-type colonies was 1:1 at 0 hours but increased to 20:1 at 24 hours post phagocytosis [6].

Anatomical context of CRSP3

• Studies on the functions of Sur2 with mouse embryonic fibroblasts (MEFs) showed that there was a multiplicity-dependent growth defect of MAV-1 in Sur2(-/-) MEFs compared to Sur2(+/+) MEFs [2].
• We demonstrate that in activated microglia the K(ATP) channel components SUR-1 or SUR-2 are present together with glucokinase [7].

Associations of CRSP3 with chemical compounds

• Glibenclamide and glimepiride, on the other hand, block channels containing SUR1 and SUR2 with similar affinity [8].

Other interactions of CRSP3

• CRSP-2 has been identified in the pig and dog, and CRSP-3 has been identified only in the pig [9].

References