Subsystem: eukaryotic rRNA modification and related functions

This subsystem's description is:

For more information, please check out the description and the additional notes tabs, below

DiagramFunctional RolesSubsystem SpreadsheetAdditional Notes 

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Group Alias
Abbrev.Functional RoleReactionsScenario ReactionsGOLiterature

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Notes copied from Eukaryotic_ribosome:
Cirhin clusters with mitoch. functions in insect genomes
Conserved oligomeric Golgi complex component 8 and NIP7-fusion in Xenopus
Treacle protein-cluster with S14e in mammals (do not come as cluster in this spreadsheet.
Cirhin-cluster with hyaluronan sysnthase in ammals

Biochem Biophys Res Commun. 2002 Mar 8;291(4):829-37. Links
Hyaluronan binding protein 1 (HABP1)/C1QBP/p32 is an endogenous substrate for MAP kinase and is translocated to the nucleus upon mitogenic stimulation.Majumdar M, Meenakshi J, Goswami SK, Datta K.
Biochemistry Laboratory, Jawaharlal Nehru University, New Delhi-110 067, India.

The role of hyaluronan binding protein 1 (HABP1) in cell signaling was investigated and in vitro kinase assay demonstrated that it is a substrate for MAP kinase. Phosphorylation of endogenous HABP1 was also observed following treatment of J774 cells with PMA. HABP1 was coimmunoprecipitated with activated ERK, confirming their physical interaction in the cellular context. Upon PMA stimulation of normal rat fibroblast (F111) and transformed (HeLa) cells, the HABP1 level in the cytoplasm gradually decreased with a parallel increase in the nucleus. In HeLa cells, within 6 h of PMA treatment, HABP1 was completely translocated to the nucleus, which was prevented by PD98059, a selective inhibitor of ERK. We also observed that the nuclear translocation of HABP1 is concurrent with that of ERK, suggesting that ERK activation is a requirement for the translocation of HABP1. It is thus established for the first time that HABP1 is a substrate for ERK and an integral part of the MAP kinase cascade.

PMID: 11866440 [PubMed - indexed for MEDLINE]

Cyclin G is aalso induced by p53(Cancer Res. 2006 Mar 15;66(6):3137-44.)