, 1991 and Park et al., 2008). The optic nerve differs from other CNS areas in several respects, however. First, it is a pure axonal tract (no gray matter). Second, in distinction to most spinal axons, the vast majority (>99%) of retinal ganglion cells die after optic nerve transection, a far greater proportion than the number of degenerating neuronal cell bodies that give rise to axons traversing a spinal cord lesion site. This raises the possibility that a unique biological feature of a subset of surviving retinal ganglion axons is the actual subject of study. The simplicity of the

optic projection to thalamic and collicular targets is a virtue: the nerve consists essentially of a single projection to few targets. If an optic nerve lesion is complete, then there is little question that regeneration has occurred. However, its simplicity is also a drawback: the optic nerve model poorly replicates see more Trichostatin A the diverse and complex nature of a spinal cord injury, which by virtue of containing both gray and white matter results in hemorrhagic necrosis, extensive inflammation, and secondary cell death and cavitation. Moreover, the complex circuitry of the spinal cord presents a diversity of inappropriate targets through which growing axons must hypothetically navigate before restoring useful function. Thus, the primary strength of the optic nerve model may

lie in understanding fundamental mechanisms underlying axonal degeneration and regeneration, leading to the identification of targets that can then be tested in models of SCI (Kurimoto et al., 2010 and Park et al., 2008). The model is discussed Maltase in more detail in other reviews (Benowitz and Yin, 2008 and Maclaren and Taylor, 1997). Studies of peripheral nerve injury have been invaluable in identifying neural mechanisms that underlie successful regeneration (Griffin et al., 2010, Longo et al., 1984, Ma et al.,

2011 and Ramon y Cajal, 1928); peripheral nerve injury models continue to yield important findings in the field (Ma et al., 2011 and Mantuano et al., 2011). The difference in perception between investigators studying central versus peripheral axonal regeneration can be amusing, as peripheral nerve investigators highlight the incompleteness and limitations in axonal regeneration after injury, whereas spinal cord investigators relish the day that growth of central axons will begin to approach the intrinsic capabilities of peripherally injured axons. As noted early in this monograph, there is also often a gulf in the use of the terms “growth,” “sprouting,” and “regeneration” as applied in the peripheral nerve literature and the CNS. A review of peripheral nerve models is beyond the scope of this Primer and interested readers are referred to recent reviews (Griffin et al., 2010 and Zochodne, 2012).

Furthermore, the protein level of synaptophysin, a cargo of KIF1A, was also increased in BDNF-treated neurons (BDNF-treated/nontreated ratio: 1.20 ± 0.04, p = 0.0077, two-tailed t test) ( Figure S4B), consistent

with previous reports ( Suzuki et al., 2007). In all experiments, there were no changes in KIF5B levels among groups ( Figures 4A–4C). In contrast to cultured neurons, no significant increase in KIF1A levels was observed in BDNF-treated astrocytes, compared with nontreated astrocytes (BDNF-treated/nontreated ratio: 1.05 ± 0.07, p = 0.5958, two-tailed t test) ( Figure S4C), suggesting that BDNF enhances KIF1A levels in neurons rather than in glial cells. Next, to study the possible effects of BDNF on KIF1A-mediated axonal transport, we analyzed the transport of synaptophysin-containing vesicles by live imaging. Time-lapse recordings revealed that the frequency of anterogradely selleck screening library transported vesicles was significantly increased in BDNF-treated neurons (nontreated versus BDNF-treated [vesicles/min]: 3.03 ± 0.34 versus 4.33 ± 0.41, p = 0.0193, two-tailed

t test) (Figures 4E and 4F and Movie S1), while the velocity was not affected (nontreated FK228 order versus BDNF-treated [μm/s]: 0.91 ± 0.06 versus 0.94 ± 0.05, p = 0.7054, two-tailed t test) (Figure 4G). In retrograde transport, there were no significant differences between BDNF-treated and nontreated neurons (nontreated versus BDNF-treated: frequency [vesicles/min], 2.23 ± 0.27 versus 2.40 ± 0.32, p = 0.6929; velocity [μm/s], 0.92 ± 0.07 versus 0.87 ± 0.05, p = 0.5804, two-tailed t test) (Figures 4F and 4G). These results suggest that BDNF augments KIF1A-mediated cargo transport by increasing the levels of KIF1A in neurons. BDNF regulates synaptic plasticity and promotes synapse formation in vivo and in vitro (Bramham and Messaoudi, 2005, Bamji et al., 2006 and Suzuki et al., 2007); therefore, to directly examine

the role of KIF1A in BDNF-induced synaptogenesis, we performed immunocytochemistry using Kif1a+/− and Kif1a−/− hippocampal neurons, with or without BDNF treatment. We quantified the densities of synaptophysin-positive puncta ( Figure 5A), PSD-95-positive puncta ( Figure 5B), and synaptophysin/PSD-95-double-positive Non-specific serine/threonine protein kinase puncta ( Figure 5C) along dendrites. BDNF treatment significantly increased the densities of synaptophysin-positive puncta (nontreated versus BDNF-treated [per 10 μm]: 1.38 ± 0.09 versus 2.32 ± 0.10, p < 0.0001, two-tailed t test) ( Figure 5D), PSD-95-positive puncta (0.96 ± 0.06 versus 1.44 ± 0.08, p < 0.0001, two-tailed t test) ( Figure 5E), and double-positive puncta (0.90 ± 0.06 versus 1.25 ± 0.09, p = 0.0026, two-tailed t test) ( Figure 5F) in wild-type neurons, as previously described ( Bamji et al., 2006 and Suzuki et al., 2007).

10 Hepatic synthesis of GSH, which is Libraries directly suppressed within the first few hours following ingestion of hepatotoxic dose of paracetamol, is overwhelmed and manifestations of toxicity appear when GSH level falls below 30% of normal. 11 When more NAPQI is formed than the available GSH for conjugation, the unbound NAPQI becomes toxic by binding to macromolecules, including cellular proteins and DNA. 12 Ecbolium viride (Forssk.) Alston commonly known as Nakka

Toka in Telugu, Udajat in Hindi, Kappu bobbili in Kannada belongs to the family Acanthaceae. E. viride is an erect glabrous herb, Z-VAD-FMK ic50 found occasional in plains of India and also found in Arabia, Sri Lanka and tropical Africa. All parts of the plant are used for gout and dysuria. 15 Decoction of the leaves is given for stricture and the roots of the plant are reported to be used for jaundice, menorrhagia and rheumatism. 13 and 14 The roots and leaves together are used against tumors. 15 It is also reported that plant possess antimicrobial, anti-inflammatory and free radical scavenging activity. The roots are reported to contain glycoflavones such as Orientin, Vitexin, Isoorientin, and Isovitexin. 16 A lignin Ecbolin A has been

isolated from the chloroform extract of root. 17 Considering the traditional AZD8055 concentration uses of this herb and the reported chemical constituents in this herb, the present study was aimed to evaluate the hepatoprotective potential of ethanolic extract of E. viride root. The Roots of E. viride (Forssk.) Alston (Acanthaceae), procured from local market of Tirupati, Andhra Pradesh, India, in August 2010, were authenticated by Dr. K. Madhava Chetty, (Assistant professor, Department of Botany) Sri Venkateshwara University, Tirupati, Andhra Pradesh, India. The voucher specimen (001/Hari) was submitted in the Department of Pharmacognosy; Deccan School of Pharmacy, Hyderabad, Andhra Pradesh, India. The E.

(-)-p-Bromotetramisole Oxalate viride (Forssk.) Alston roots were air dried in shade and were made to coarse size. The coarse sized roots were subjected to extraction by using the Soxhlet apparatus. These coarse sized roots were defatted with petroleum ether for 72 h on 40–50 °C temperature. Then alcoholic extraction with ethyl alcohol was done 44–48 h at 40–50 °C temperature. After extraction, solvent was recovered by distillation. The concentrated extract was dried on water bath at 40–50 °C, made in powder form and the yield was 2.66% w/w. Phytochemistry of the ethanolic extract was carried out using the method of Khandelwal.18 The result indicated the presence of glycosides, alkaloids, saponins, flavonoids, and tannins. Healthy adults Albino Wistar rats (100–150 g each) aged 60–90 days were used for the study. The rats were housed in polypropylene cage and maintained under standard conditions (12 h light/12 h dark cycle; 25 ± 3 °C; 35–60% humidity). Standard pelletized feed and tap water were provided ad libitum.

The use of prevention of colonization as a biologically functional endpoint makes clinical field assessments (phase

III or IV) smaller, less costly, faster and technically feasible in a wide variety of locations. Therefore it can be used to assess not only new vaccine formulations but also address vaccine dosage and schedules relevant to buy BGJ398 the local vaccination programs. We also argue that it is a critical method for documenting PCV impact at the individual and community level following introduction into the routine immunization programs of countries; although it is not a disease endpoint in itself, where IPD surveillance is limited or not possible, colonization impact reveals the biologic impact of the vaccine on the organism and by bridging to other data where both IPD and colonization have been assessed, will allow for inferences about disease impact. Therefore, the Staurosporine ic50 specific PneumoCarr project goals were to (1) develop the use of vaccine efficacy against pneumococcal nasopharyngeal

colonization (VE-colonization) as part of the regulatory Libraries licensure process, and (2) determine recommendations for how to optimally use NP colonization evaluations to inform the impact of PCV vaccines for public health purposes. The project objectives to meet these goals were to (1) develop the scientific basis and analytic Adenylyl cyclase tools for pneumococcal colonization studies as a supportive strategy for licensure, and (2) develop and support the technical community understanding and acceptance of pneumococcal colonization as an approach to licensure of novel pneumococcal vaccines. These two objectives address the key obstacles

to use of VE-colonization as a strategy for the development, licensure and implementation of new pneumococcal vaccine products. An international consultation “Workshop to explore the role of carriage studies in the evaluation and licensing of new pneumococcal vaccines”, co-sponsored by WHO and PneumoCarr, was convened at WHO in Geneva, Switzerland, in March 2012 to provide vaccine manufacturers and regulators the opportunity to understand and comment on the “Case for Carriage, C4C” document, a PneumoCarr white paper that presents the justification for the inclusion of VE-col in pneumococcal vaccine licensure pathway.

One study of a 30-minute walk/jog regimen 3 days per week found a benefit for dysmenorrhoea,33 although it was not eligible

for this review because the outcome was a composite symptom score. Although the analgesic benefits of heat, TENS, and yoga were statistically significant, the evidence for each intervention came with minor caveats. All estimates were provided by only a single trial, the confidence interval did not exclude the possibility that the effect was clinically trivial, and the quality of the trial was low. However, these interventions have relatively low costs and risks, so some women with dysmenorrhoea may wish to try them despite these uncertainties. This systematic review has several strengths. Two reviewers independently performed study selection, quality assessment, and data

extraction. Statistically significant benefits were identified Trichostatin A clinical trial for several interventions. Important insights into placebo effects were identified by the separation of sham-controlled Modulators trials from trials with no-treatment controls. A possible limitation is that the search did not include grey literature, which is more likely to report no statistical significance between groups.34 and 35 This may temper the positive nature of the evidence of efficacy reported in this review. Although there was also potential for language bias, the 13 non-English, non-Swedish articles were excluded for other reasons during the abstract screening. Therefore, Staurosporine language bias was not a limitation. The average PEDro score was within the range we nominated

as high quality, and the rarely achieved blinding items on the PEDro scale were met, with blinding of participants (5 trials), assessors (4 trials), and therapists (2 trials). In conclusion, this review identified that heat, TENS, and yoga can each significantly reduce the pain of dysmenorrhoea. The magnitude of these effects may or may not be 17-DMAG (Alvespimycin) HCl clinically worthwhile, but as the costs and risks of these interventions are low, they could be considered for clinical use. The review also identified moderate-grade evidence to support the use of acupuncture and acupressure, although this may be due to a placebo effect. Although one study identified a part from spinal manipulation, the weight of evidence was that it was not effective. Data from further research on these and other interventions, such as whole body exercise, could help to provide more precise estimates of the average effects of physiotherapy interventions for dysmenorrhoea. What is already known on this topic: Many women of reproductive age experience dysmenorrhea. Although medications are available to treat the pain, these produce side effects or incomplete pain relief in a substantial proportion of women with dysmenorrhea. Several physiotherapy interventions have been investigated as non-pharmacological interventions for dysmenorrhea.

All participants were reviewed fortnightly by an unblinded therapist, who contacted them either by phone or in person to monitor and record adherence to their programs. The splint intervention was ceased following assessments at 8 weeks, and all participants continued with the

exercises and advice unsupervised until 12 weeks. Outcomes were measured immediately before randomisation (ie, baseline) and then at 8 weeks, with a follow-up measure at 12 weeks after randomisation. A blinded assessor performed assessments at 8 weeks, at least 12 hours after the splint was last worn; an assessor not blinded to group allocation performed assessments at 12 weeks. The success of blinding at 8 weeks was examined using an assessor questionnaire administered at the completion of each participant’s Libraries assessment. Eight SNS-032 datasheet outcome measures were used. The two primary outcome measures reflected impairment and participation restriction, namely: passive wrist extension, and the Patient Rated Hand Wrist

Evaluation (PRHWE). Secondary outcome measures were active wrist extension, flexion, radial and ulnar deviation, and the performance and satisfaction items of the Canadian Occupational Performance Measure (COPM). The details of each follow. Passive wrist extension: Passive wrist extension was measured with the application of a standardised torque using a device specifically designed for this purpose ( Figure 2). The device consisted of a wheel mounted on the ATM Kinase Inhibitor mw side of an arm board that was hinged to a mobile plate. With the device on a horizontal surface, the hand was strapped to the mobile plate rotating

about the axis of the wrist with the forearm pronated. The fingers were allowed to lie over the distal end of the plate to prevent finger flexor tightness confounding the measurement. The wheel acted to ensure the moment arm remained constant (9 cm) regardless of wrist angle. 250 g weights were serially added with 30 seconds of pre-stretch until a final weight of 1.25 kg was reached, corresponding to 0.22 Nm increments in torque with a final torque of 1.10 Nm. Passive wrist extension was measured as the angle between the mobile plate and Non-specific serine/threonine protein kinase a vertical drop-line 30 seconds after the application of the final torque. The reliability of the device was evaluated before the commencement of the trial by having two assessors measure the passive wrist extension of 11 people with contracture following fracture. An ICC of 0.98 (95% CI, 0.96 to 0.99) was established. A between-group difference of 10 deg was deemed sufficiently important to justify the expense and inconvenience of the splinting regimen. Patient Rated Hand and Wrist Evaluation(PRHWE): The PRHWE ( MacDermid and Tottenham 2004) is a 15-item questionnaire designed to reflect the implications of upper limb injuries on activities of daily living.

, 1999) ( Figure S3C). Exposure to enrichment for 3 weeks significantly increased hippocampal neurogenesis in wild-type mice (nonenriched versus enriched [normalized to nonenriched Dolutegravir purchase wild-type]: 1.00 ± 0.08 versus 1.71 ± 0.20, p = 0.0302, two-tailed t test) ( Figure S3D), consistent with previous reports ( Kempermann et al., 1997 and van Praag et al., 1999). Compared with nonenriched wild-type mice, nonenriched Bdnf+/− mice showed reduced neurogenesis (wild-type versus Bdnf+/− [normalized to nonenriched wild-type]:

1.00 ± 0.08 versus 0.69 ± 0.04, p < 0.05, post hoc Dunnett's test) ( Figure S3D), as previously reported ( Lee et al., 2002 and Sairanen et al., 2005). In contrast to wild-type mice, Bdnf+/− mice did not show any increase in neurogenesis after enrichment (nonenriched versus enriched [normalized to nonenriched wild-type]: 0.69 ± 0.04 versus 0.79 ± 0.08, p = 0.3792, two-tailed t test) ( Figure S3D). This result is consistent with

previous reports ( Rossi et al., 2006). Meanwhile, neurogenesis of nonenriched Kif1a+/− mice was comparable to that of nonenriched wild-type Selleckchem EPZ 6438 mice (wild-type versus Kif1a+/− [normalized to nonenriched wild-type]: 1.00 ± 0.08 versus 1.04 ± 0.10, p > 0.05, post hoc Dunnett’s test) ( Figure S3D). Interestingly and consistent with wild-type mice, Kif1a+/− mice exhibited enhanced hippocampal neurogenesis after enrichment (nonenriched versus enriched [normalized to nonenriched wild-type]: 1.04 ± 0.10 versus 1.58 ± 0.16, p = 0.0450, two-tailed t test) ( Figure S3D). These results suggest that KIF1A is not required for enhanced hippocampal

neurogenesis induced by enrichment. To analyze the possible BDNF-dependent upregulation of KIF1A in more detail, we first examined the effects of BDNF on KIF1A levels in cultured hippocampal neurons. Quantitative immunoblot analyses revealed that there was an increase in KIF1A levels in BDNF-treated neurons in a time-dependent (BDNF-treated/nontreated ratio: 1 day, 1.19 ± 0.07, p = 0.0471; 3 days, 1.62 ± 0.07, p < 0.001; 5 days, 1.67 ± 0.05, p < 0.001, two-tailed t test) (Figure 4A) and dose-dependent manner (BDNF concentration [ng/ml], ratio to Amisulpride 0 ng/ml: 10 ng/ml, 1.40 ± 0.05, p = 0.0016; 50 ng/ml, 1.55 ± 0.05, p < 0.001; 100 ng/ml, 1.64 ± 0.07, p < 0.001; 200 ng/ml, 1.67 ± 0.07, p < 0.001, two-tailed t test) (Figure 4B). This upregulation of KIF1A was completely blocked by K252a, a general inhibitor of Trk tyrosine kinase (BDNF+K252a-treated/non-treated ratio: 1.02 ± 0.06, p = 0.6843, two-tailed t test) (Figure 4C). The level of Kif1a mRNA was also increased (BDNF-treated/non-treated ratio: 1 day, 1.22 ± 0.05, p = 0.0487; 3 days, 1.64 ± 0.04, p = 0.0047; 5 days, 1.70 ± 0.07, p = 0.

Hebbian models of the V1 circuit that incorporate the smaller ocular dominance shift of inhibitory neurons after brief MD provide a potential explanation of the requirement for a threshold level of inhibition for ODP (Gandhi et al., 2008 and Yazaki-Sugiyama et al., 2009). It is not yet clear what differences among mouse strains, inhibitory cell types, or techniques account for the inconsistency in inhibitory neuron responses between the three studies. In monkeys and cats, transneuronal labeling revealed a shrinkage of deprived-eye and complementary expansion of open-eye thalamocortical projections

(Hubel et al., 1977). However, thalamocortical axon rearrangement is Selleck 3Methyladenine much too slow to explain the rapid shift of ocular dominance during the critical period (Antonini and Stryker, 1993b). Indeed Adriamycin mouse in cats, responses of neurons in layer 4 have not begun to shift at 1–2 days MD when ocular dominance changes in layers 2–3 are nearly saturating (Trachtenberg et al., 2000). This slower shift of ocular dominance in layer 4 parallels thalamocortical anatomical changes (Antonini and Stryker, 1993b). In contrast, anatomical changes in the upper layers of cortex are much more rapid: strabismus dramatically reduced horizontal connectivity

between columns representing the two eyes in less than 2 days (Trachtenberg and Stryker, 2001). Similarly, 4 days of MD had no effect on spine density PDK4 in layer 4 spiny stellate neurons (Lund et al., 1991). Interestingly, the difference in timing between ODP in layer 2/3 and layer 4 may not apply to the mouse (Liu et al., 2008), in which thalamic inputs from the two eyes are intermingled in layer 4. In this situation, axon growth or retraction may

not be required to find postsynaptic partners dominated by the other eye. This may also explain why rodents show more plasticity in adult life than do animals with a columnar cortical organization of V1 (Lehmann and Löwel, 2008). Structural and functional measurements can now delineate the inputs that give rise to specific response properties of different cell types in V1 (Reid, 2012). Two-photon laser scanning imaging in mice also allows one to follow structural changes longitudinally during ODP. In critical period transgenic mice expressing GFP in a subset of layer 5 cells (thy1-GFP line M) (Feng et al., 2000), the motility of spines in layers 2, 3, and 5, but not 4 was elevated by 2 days of MD (Oray et al., 2004), consistent with early extragranular changes that instruct later events in layer 4 (Trachtenberg et al., 2000). Since this effect was observed only in the binocular zone of V1, it probably reflects a competitive mechanism related to ODP. In adult thy1-GFP line M mice, MD caused the addition of dendritic spines on the apical tufts of layer 5 but not layer 2/3 pyramidal neurons (Hofer et al., 2009).

2) with post hoc tests indicating a significant Panobinostat cost increase in the vibration group (p < 0.05) ( Fig. 3). There was no time × group interaction for the 505 agility test (p > 0.05) although, similar to the DJH data, there was a trend towards the vibration intervention

having a greater negative effect on agility (increased time) than the other interventions. The current study is the first to look at the effects that the addition of WBV to the FIFA 11+ has on RSI and 505 agility. The aim of the present research was to investigate the benefits of including an acute bout of vibration stimulus following the FIFA 11+ in collegiate soccer players. A well established and successful warm-up has not only benefits to subsequent performance,5, 6 and 7 but also injury prevention.8 The FIFA 11+ has been recognised as a well-established tool for reducing injury Paclitaxel order rates amongst soccer players, however performance improvements following its intervention have not been reported as clearly.1, 9 and 10 From the present results the addition of acute vibration to well-established warm-up has shown positive results in RSI through a decrease in CT, however there

was no improvement in 505 agility amongst participants. Factors such as reactive strength have been strongly correlated to change of direction efficiency and speed,37 as well as a key distinguishing characteristic between elite and non-elite soccer players.38 Such acute improvements in these characteristics should therefore welcomed by players and coaches. The determination of physiological mechanisms responsible for the significant acute changes that took place following different warm-up protocols is beyond its scope of the present study as no direct neuromuscular responses were measured. The changes in RSI however indicate that there has been a neuromuscular response due to WBV which will be discussed and suggestions made to why this may have occurred. As identified in previous

research one potential explanation for the improvements in RSI (through a reduction in contact time) is due to increased efficiency in the stretch shortening cycle (SSC).24 In particular an improvement in the short-latency stretch reflex would mean a significant reduction in CT, as this corresponds Astemizole to the reflex after ground contact.39 Vibration training as a mechanical stimulus has been linked to an improvement in latency stretch reflex post vibration.40 and 41 Increased muscle spindle sensitivity and a decrease in recruitment threshold of motor units could also be suggested as a key factor for the decreases in CT,42 with an increase in spindle sensitivity improving detection on landing and a lowering of recruitment threshold meaning an increase in the velocity of contraction.42 The above argument however, of an increase in short-latency stretch reflex and a decrease in recruitment threshold are questioned by the current findings. Such neuromuscular changes could also benefit the 505 agility time but this was not the case.

The Aβ plaque-specific

mE8 antibody might be an attractive candidate therapy to consider for secondary prevention trials for individuals with preclinical AD as well as for treatments of individuals with very mild dementia due to AD. Since those with preclinical AD and mild cognitive impairment or very mild dementia KU-57788 chemical structure due to AD already have substantial Aβ deposition in their brain (Jack et al., 2010; Perrin et al., 2009), this type of treatment targeting pre-existing Aβ plaques might be quite promising as a disease modifying treatment. D.M.H. is a cofounder and on the Scientific Advisory Board of C2N Diagnostics. In the last year, he served as a neuroscience therapeutic area Scientific Advisor to Pfizer. “
“Neurons are some of the most complex and highly polarized cells in our body. Their complex dendritic morphologies underlie their ability to integrate synaptic inputs. For this reason, the mechanisms that drive dendritic morphogenesis have been extensively

studied over recent decades (reviewed Whitford et al., 2002). Cytoskeletal dynamics are required for proper formation and maintenance of both dendritic and axonal branches (reviewed Kobayashi and Mundel, 1998; Gallo, 2011). The cytoskeleton is composed of microtubules (MTs), 3-Methyladenine molecular weight actin filaments, intermediate filaments, and a myriad of regulators that process, order, modify, and remove these structures in a dynamic way. MTs are the largest and longest of these filaments, and are formed by polymerization of α- and β-tubulin dimers. This polymerization

gives rise to an inherent polarity along microtubules with a plus-end (where new dimers are polymerized) and a minus-end (where dimers are depolymerized) (reviewed Baas and Lin, 2011). The site at which microtubules are nucleated in neurons has Tolmetin been an important open question. This has been widely studied in nonneuronal cell types, but because of technical limitations is only recently being addressed in neurons. We have learned from nonneuronal cell types that microtubules are often nucleated at the microtubule-organizing center (MTOC), which is coupled to the centrosome. However, microtubules can also be nucleated from the nuclear envelope, melanosomes, plasma membrane, and the Golgi complex in a process called acentrosomal nucleation (reviewed Vinogradova et al., 2009). MT nucleation at the Golgi has received recent attention as it provides asymmetry in the MT arrays of motile cells and might be important for cell polarization. Four main proteins are thought to be responsible for the MT nucleating ability of the Golgi: γ-tubulin, AKAP450, GM130, and CLASPs, which provide a molecular scaffold for the MT nucleation process (Kollman et al., 2010; Rivero et al., 2009; Efimov et al., 2007).