Disease relevance of Stmn1

• We conclude that stathmin expression in demyelinating disorders could have a dual role [1].
• Stathmin immunoreactivity was also associated with neurons undergoing ectopic chain migration into the ischemic striatum and cerebral cortex following focal cerebral ischemia [2].
• In this study, we report the increased expression of stathmin, a developmentally regulated tubulin-binding protein, in the brains of patients with multiple sclerosis (MS) [1].
• RT-PCR and ISH analyses indicated that the expression of RB3 was specifically increased in the ganglion cell layer (GCL) comparing to other members of stathmin-related gene family examined 3 days following the ON axotomy [3].
• Several of the altered proteins, including hsp27, hsp86 and stathmin, may ultimately serve as markers of early breast cancer development [4].

High impact information on Stmn1

• Stat3 regulates microtubules by antagonizing the depolymerization activity of stathmin [5].
• In addition, down-regulation of stathmin protein levels in Stat3-deficient cells partially reversed the MT and migration deficiencies [5].
• Furthermore, we found that stathmin phosphorylation in PC12 cells which is induced by NGF depends on mitogen-activated protein kinase (MAPK) activity [6].
• Stathmin is a ubiquitous cytosolic protein which undergoes extensive phosphorylation in response to a variety of external signals [6].
• We show that stathmin depletion prevents nerve growth factor (NGF)-stimulated differentiation of PC12 cells into sympathetic-like neurons although the expression of several NGF-inducible genes was not affected [6].

Biological context of Stmn1

• As proof of the principle that this approach could identify genes whose upregulation was necessary for nonadherent growth, we investigated one gene, stathmin whose upregulation by cJun was observed only under these conditions [7].
• By two-dimensional electrophoresis, phosphorylation of Op18/stathmin was found to be increased upon the expression of constitutively active ASK1 (ASK1DeltaN) in PC12 cells [8].
• Stathmin expression clearly increases in the uterus when stimulated by embryo implantation and decidualization and may play a role in the early stages of pregnancy [9].
• In physiological conditions, stathmin immunoreactivity was observed in polysialic acid-neural cell adhesion molecule-positive migratory progenitors in the subventricular zone, and its expression progressively decreased as the cells matured into oligodendrocytes (OLs) [1].
• Neuronal activity induction of the stathmin-like gene RB3 in the rat hippocampus: possible role in neuronal plasticity [10].

Anatomical context of Stmn1

• At the molecular level, each possesses a specific "stathmin-like domain" and, with the exception of stathmin, various combinations of N-terminal extensions involved in their association with intracellular membrane compartments [11].
• Stathmin mRNA was highly expressed both in the RGCs and other interneurons [12].
• In situ hybridization revealed that GAP-43 and all of the SCG10-related family mRNAs were present in the retinal ganglion cells (RGCs) at all stages of retinal development, and that stathmin mRNA was present in mitotic neuroblastic cells [12].
• Phosphoproteins of the stathmin family are important regulators of microtubule dynamics, in particular in the developing and mature nervous system [13].
• Two separate motifs cooperate to target stathmin-related proteins to the Golgi complex [13].

Associations of Stmn1 with chemical compounds

• Consistently, we found that all four isoforms of p38 directly phosphorylated Op18/stathmin primarily at serine 25 in vitro [8].
• In the delayed implantation pregnant rat model, uterine stathmin expression was low, but increased after implantation induced by administration of 17beta-estradiol to the progesterone-primed animal [9].
• Stathmin is one of the major neural-enriched cytosolic phosphoproteins and a potential target of cyclic-AMP-dependent kinases [Jin L. W. et al. (1996) Neurobiol. Aging 17, 331-341; Leighton I. A. et al. (1993) Molec. Cell Biochem. 127/128, 151-156] [14].
• In this review, the neuroprotective actions of testosterone on three different populations of injured rat peripheral motoneurons, i.e. facial (FMN), spinal (SMN) and pudendal (PMN), will be discussed [15].
• We previously reported that when 32Pi-loaded rat parotid slices are incubated with the beta-adrenergic agonist isoproterenol, the level of a soluble 32P-labeled 17-kDa protein (pp17) decreases rapidly (Kanamori, T., and Hayakawa, T. (1982) Biochem. Int. 4, 517-523) [16].

Physical interactions of Stmn1

• Modulation of the stathmin-like microtubule destabilizing activity of RB3, a neuron-specific member of the SCG10 family, by its N-terminal domain [17].
• In this study, we show that clusterin interacts with the microtubule-destabilizing stathmin family protein SCLIP by GST pull-down and co-immunoprecipitation assays [18].

Enzymatic interactions of Stmn1

• KIS produced in bacteria has an autophosphorylating activity and phosphorylates stathmin on serine residues [19].

Regulatory relationships of Stmn1

• Electrophoretic studies on the phosphorylation of stathmin and mitogen-activated protein kinases in neuronal cell death induced by oxidized very-low-density lipoprotein with apolipoprotein E [20].
• The cytosolic phosphoprotein stathmin is expressed in the olfactory system of the adult rat [21].

Other interactions of Stmn1

• These results suggest that stathmin plays an essential role in anchorage-independent growth by cJun and may be a potential target for specific inhibitors for AP-1-dependent processes involved in carcinogenesis [7].
• The pattern of expression of the RB3 transcript is very different from that of the three other members of the stathmin family [22].
• Stathmin immunohistochemistry in adult rodent brain revealed prominent expression in neuroproliferative zones and neuronal migration pathways, a pattern that resembles the expression of doublecortin, which is implicated in neuronal migration [2].
• SCG10 and stathmin expression in the olfactory receptor neurons was found to be regulated during embryonic and postnatal development and to correlate with neuronal maturation [23].
• Accordingly, it is most likely that caveolin increased the polymer form of microtubule through the inhibition of a microtubule destabilizer, stathmin, suggesting a novel role of caveolin in regulating cellular network and trafficking [24].

Analytical, diagnostic and therapeutic context of Stmn1

• Northern blot analysis as well as in situ hybridization experiments showed that all stathmin-related mRNAs are expressed in a wide range of adult rat brain areas [22].
• To examine possible roles of SCG10 in the adult brain, we examined the distribution of messenger RNAs encoding SCG10 and p19/stathmin as well as GAP-43 in adult rat brain sections by northern blot, RNase protection and in situ hybridization [25].
• To examine the distribution of stathmin-related gene products, we performed semi-quantitative reverse transcription polymerase chain reaction (RT-PCR), in situ hybridization (ISH) and immunohistochemical analyses [3].
• In this study, we examined the cellular responses of stathmin-related proteins in the rat retina following optic nerve (ON) axotomy [3].
• After two-thirds partial hepatectomy, the concentration of stathmin reached a peak between 48 and 72 hours, comparable to the levels observed in neonatal liver, at about 10 times the basal adult level [26].

References