The reference OMIM entry for this protein is 600621

Stathmin-like 2; stmn2
Superior cervical ganglia, neural specific, 10; scgn10
Superior cervical ganglion 10; scg10
Neuronal growth-associated protein scg10

DESCRIPTION

STMN2 is a neuronal growth-associated protein that shares significant amino acid sequence similarity with the phosphoprotein stathmin (STMN1; 151442) (Okazaki et al., 1993).

CLONING

The rat SCG10 cDNA was cloned by Stein et al. (1988), and Okazaki et al. (1993) isolated most of the mouse gene. The predicted amino acid sequences of SCG10 in the 2 species differ by a single residue (see erratum for Okazaki et al., 1993). The mouse Scgn10 transcription unit spans at least 30 kb, while the stathmin gene is 6 kb long. Both genes have 5 exons. Southern blot analysis indicated that Scgn10 is encoded by a single gene in the mouse that is linked to Il7 in the proximal region of chromosome 3. Okazaki et al. (1993) suggested that in contrast to the more broadly expressed stathmin gene, the neuron-specific SCG10 gene may have evolved by duplication and acquisition of a tissue-specific promoter.

GENE FUNCTION

Schoenherr and Anderson (1995) cloned a transcription factor, which they termed neuron-restrictive silencer factor (NRSF; 600571), that repressed transcription of SCG10 by binding to a 24-bp regulatory element, called the neuron-restrictive silencer element (NRSE), located in the distal 5-prime regulatory region of the gene. Using indexing-based differential display PCR on neuronal precursor cells to study gene expression in Down syndrome (190685), Bahn et al. (2002) found that genes regulated by the REST (600571) transcription factor were selectively repressed. One of these genes, SCG10, was almost undetectable. The REST factor itself was also downregulated by 49% compared to controls. In cell culture, the Down syndrome cells showed a reduction of neurogenesis, as well as decreased neurite length and abnormal changes in neuron morphology. The authors noted that REST-regulated genes play an important part in brain development, plasticity, and synapse formation, and they suggested a link between dysregulation of REST and some of the neurologic deficits seen in Down syndrome. Using immunohistochemistry, Greka et al. (2003) showed that stathmin-like-2 colocalized with the transient receptor potential cation channel TRPC5 (300334) in cytoplasmic transport vesicles along hippocampal neuronal processes and in the growth cone. In cells transfected with mutant stathmin-like-2, the TRPC5 signal was significantly reduced, and the authors suggested that stathmin-like-2 is required for loading of TRPC5 in the transport vesicles. A dominant-negative form of TRPC5 allowed significantly longer neurites and filopodia to form, indicating that TRPC5 may regulate neuronal growth. Greka et al. (2003) noted that influxes of calcium via voltage-gated channels play a role in neuronal outgrowth and suggested that TRPC5 is a candidate for the regulation of calcium waves. By yeast 2-hybrid analysis of an embryonic mouse cDNA library, Alves et al. (2010) found that Kbp (KIAA1279; 609367) interacted with the microtubule-destabilizing protein Scg10, with tubulin alpha-7 (Tuba3b), and with several kinesins. Coimmunoprecipitation analysis of transfected HEK293 cells and colocalization of Kbp and Scg10 in N1E-115 cells confirmed the interaction between Kbp and Scg10. Kbp did not appear to interact directly with microtubules. Knockdown of Kbp expression in rat PC12 cells inhibited NGF-beta (NGFB; 162030)-induced neurite outgrowth. Alves et al. (2010) concluded that KBP has an indirect role in regulating microtubule dynamics and neur ... More on the omim web site

Subscribe to this protein entry history

June 30, 2020: Protein entry updated
Automatic update: OMIM entry 600621 was added.

Oct. 19, 2018: Additional information
Initial protein addition to the database. This entry was referenced in Bryk and co-workers. (2017).