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Gene Review

STMN3  -  stathmin-like 3

Homo sapiens

Synonyms: SCG10-like protein, SCLIP, Stathmin-3
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High impact information on STMN3

  • The strongest correlations were for bone marrow stromal antigen 2, stathmin-like 3, tumor necrosis factor receptor superfamily member 5, and hepatocyte growth factor tyrosine kinase substrate [1].
  • SCLIP, a Microtubule-destabilizing Factor, Interacts with RasGRF1 and Inhibits Its Ability to Promote Rac Activation and Neurite Outgrowth [2].
  • Moreover, a potential role is suggested by transfection studies in neuronal PC12 cells in which RasGRF1 induces neurite outgrowth, and coexpression of SCLIP counteracts this effect, causing a dramatic decrease in the percentage of cells bearing neurites, which also appear significantly shortened [2].
  • We examined the biological properties and functions of SCLIP, the stathmin family protein most similar to SCG10, a widely studied and recognized neuronal differentiation marker [3].
  • SCLIP, like SCG10, is present from the earliest stages of hippocampal neuron differentiation in culture at vesicle-like structures following dynamic microtubules [3].

Biological context of STMN3

  • Surprisingly, SCLIP, whose expression is thought to be neural-specific, exhibits a broader tissue distribution [4].
  • Analyses of the SCLIP gene (approved symbol STMN3) show that it contains several NRSE-like elements that display low or no affinity for the cognate binding protein NRSF [4].
  • In addition to revealing a novel function for SCLIP in axonal morphogenesis, our results demonstrate for the first time that stathmin family proteins fulfill different and complementary roles during neuronal differentiation [3].
  • Its inhibition by RNA interference resulted in increased axonal branching, revealing a novel biological role for SCLIP, distinct from SCG10 whose down-regulation in the same conditions promoted growth cone expansion [3].

Other interactions of STMN3

  • The substantial expression of SCLIP in most tissues points out a novel function for this protein outside the nervous system and raises the possibility that its coexpression with stathmin could provide some degree of functional redundancy [4].


  1. Identification of genes expressed in malignant cells that promote invasion. Walter-Yohrling, J., Cao, X., Callahan, M., Weber, W., Morgenbesser, S., Madden, S.L., Wang, C., Teicher, B.A. Cancer Res. (2003) [Pubmed]
  2. SCLIP, a Microtubule-destabilizing Factor, Interacts with RasGRF1 and Inhibits Its Ability to Promote Rac Activation and Neurite Outgrowth. Baldassa, S., Gnesutta, N., Fascio, U., Sturani, E., Zippel, R. J. Biol. Chem. (2007) [Pubmed]
  3. The "SCG10-LIke Protein" SCLIP is a novel regulator of axonal branching in hippocampal neurons, unlike SCG10. Poulain, F.E., Sobel, A. Mol. Cell. Neurosci. (2007) [Pubmed]
  4. Expression of stathmin family genes in human tissues: non-neural-restricted expression for SCLIP. Bièche, I., Maucuer, A., Laurendeau, I., Lachkar, S., Spano, A.J., Frankfurter, A., Lévy, P., Manceau, V., Sobel, A., Vidaud, M., Curmi, P.A. Genomics (2003) [Pubmed]
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