Disease relevance of Stmn2

• To explore the structural and evolutionary relationships between these genes, we have isolated a series of cosmid and phage clones that covers the entire region of the mouse stathmin gene and most of the mouse SCG10 gene [1].

High impact information on Stmn2

• Differentiation of this precursor to neurons that express markers such as SCG10, peripherin, and neuron-specific enolase is dependent upon MASH1 function [2].
• We have localized a cell type-specific silencer element in the SCG10 gene by deletion analysis [3].
• Deletion of the 5'-most 3.7 kb of SCG10 sequence yields deregulated expression of the transgene in numerous nonneuronal tissues, although expression remains highest in brain [4].
• A low level of expression is detected in adrenal gland as well, consistent with the behavior of endogenous SCG10 [4].
• SCG10 is a neural-specific, growth-associated protein that is broadly expressed in the embryonic central and peripheral nervous systems [4].

Biological context of Stmn2

• Southern blot analysis indicates that SCG10 mRNA is encoded by a single gene in the mouse genome, while stathmin cDNA probes detect multiple genes [1].
• SCG10, a protein closely related in structure to metablastin, shows no compensatory up-regulation in metablastin-/- mice [5].
• Stathmin and SCG10 belong to a family of phosphoproteins associated to cell proliferation and differentiation [6].
• The p19/SCG10 gene family encodes two structurally related cellular proteins that are implicated in signal transduction during differentiation of mammalian cells [7].
• Analysis of SCG10 gene expression in transgenic mice reveals that neural specificity is achieved through selective derepression [4].

Anatomical context of Stmn2

• Analysis of sensory neurons which strongly express NSCL-1 revealed that the spatiotemporal expression of neuronal differentiation factors, such as NeuroD and SCG-10, was not altered in developing distal and proximal cranial ganglia of mutant mice [8].
• As a first step to understanding the signaling mechanisms downstream of Pcdhgamma, we identify the microtubule-destabilizing protein SCG10 as a cytoplasmic interactor for Pcdhgamma-b1 and other isoforms of the Pcdhgamma-b subfamily, and show that SCG10 and Pcdhgamma-b1 are found together in certain neuronal growth cones [9].
• SCG10 mRNA localization in the hippocampus: comparison with other mRNAs encoding neuronal growth-associated proteins (nGAPs) [10].
• SCG10 mRNA is not detectable in the dentate gyrus of the mouse hippocampus, although it is expressed in the rat dentate gyrus [10].
• In the mouse, SCG10 mRNA is expressed at high levels in pyramidal cells of CA3-CA4 sub-fields of Ammon's horn and at low levels in the CA1-CA2 sub-fields, while it is found rather uniformly throughout the pyramidal cell layer of the rat hippocampus [10].

Regulatory relationships of Stmn2

• These data are consistent with the idea that the neuron-specific SCG10 gene evolved by duplication and modification of the more broadly expressed stathmin/Lap18 gene [1].

Other interactions of Stmn2

• Molecular diversity of the SCG10/stathmin gene family in the mouse [1].
• After regeneration in the adult following peripheral lesion of the olfactory epithelium, stathmin and SCG10 were again strongly expressed and generally colocalized with neuronal specific tubulin immunoreactivity [6].

Analytical, diagnostic and therapeutic context of Stmn2

• During the post-implantation period, SCG10 transcripts were only detected in the uterus and placenta by reverse transcriptase-PCR, whereas p19 mRNA could be detected by Northern blotting and showed stage-specific expression in both tissues [7].

References