A Cross-Source Point Cloud Registration Algorithm Based on Trigonometric Mutation Chaotic Harris Hawk Optimisation for Rockfill Dam Construction.

A high-precision three-dimensional (3D) model is the premise and vehicle of digitalising hydraulic engineering. Unmanned aerial vehicle (UAV) tilt photography and 3D laser scanning are widely used for 3D model reconstruction. Affected by the complex production environment, in a traditional 3D reconstruction based on a single surveying and mapping technology, it is difficult to simultaneously balance the rapid acquisition of high-precision 3D information and the accurate acquisition of multi-angle feature texture characteristics. To ensure the comprehensive utilisation of multi-source data, a cross-source point cloud registration method integrating the trigonometric mutation chaotic Harris hawk optimisation (TMCHHO) coarse registration algorithm and the iterative closest point (ICP) fine registration algorithm is proposed. The TMCHHO algorithm generates a piecewise linear chaotic map sequence in the population initialisation stage to improve population diversity. Furthermore, it employs trigonometric mutation to perturb the population in the development stage and thus avoid the problem of falling into local optima. Finally, the proposed method was applied to the Lianghekou project. The accuracy and integrity of the fusion model compared with those of the realistic modelling solutions of a single mapping system improved.

An Efficient Deep Learning-Based High-Definition Image Compressed Sensing Framework for Large-Scene Construction Site Monitoring.

High-definition images covering entire large-scene construction sites are increasingly used for monitoring management. However, the transmission of high-definition images is a huge challenge for construction sites with harsh network conditions and scarce computing resources. Thus, an effective compressed sensing and reconstruction method for high-definition monitoring images is urgently needed. Although current deep learning-based image compressed sensing methods exhibit superior performance in recovering images from a reduced number of measurements, they still face difficulties in achieving efficient and accurate high-definition image compressed sensing with less memory usage and computational cost at large-scene construction sites. This paper investigated an efficient deep learning-based high-definition image compressed sensing framework (EHDCS-Net) for large-scene construction site monitoring, which consists of four parts, namely the sampling, initial recovery, deep recovery body, and recovery head subnets. This framework was exquisitely designed by rational organization of the convolutional, downsampling, and pixelshuffle layers based on the procedures of block-based compressed sensing. To effectively reduce memory occupation and computational cost, the framework utilized nonlinear transformations on downscaled feature maps in reconstructing images. Moreover, the efficient channel attention (ECA) module was introduced to further increase the nonlinear reconstruction capability on downscaled feature maps. The framework was tested on large-scene monitoring images from a real hydraulic engineering megaproject. Extensive experiments showed that the proposed EHDCS-Net framework not only used less memory and floating point operations (FLOPs), but it also achieved better reconstruction accuracy with faster recovery speed than other state-of-the-art deep learning-based image compressed sensing methods.

Deep transfer learning of structural magnetic resonance imaging fused with blood parameters improves brain age prediction.

Machine learning has been applied to neuroimaging data for estimating brain age and capturing early cognitive impairment in neurodegenerative diseases. Blood parameters like neurofilament light chain are associated with aging. In order to improve brain age predictive accuracy, we constructed a model based on both brain structural magnetic resonance imaging (sMRI) and blood parameters. Healthy subjects (n = 93; 37 males; aged 50-85 years) were recruited. A deep learning network was firstly pretrained on a large set of MRI scans (n = 1,481; 659 males; aged 50-85 years) downloaded from multiple open-source datasets, to provide weights on our recruited dataset. Evaluating the network on the recruited dataset resulted in mean absolute error (MAE) of 4.91 years and a high correlation (r = .67, p <.001) against chronological age. The sMRI data were then combined with five blood biochemical indicators including GLU, TG, TC, ApoA1 and ApoB, and 9 dementia-associated biomarkers including ApoE genotype, HCY, NFL, TREM2, Aß40, Aß42, T-tau, TIMP1, and VLDLR to construct a bilinear fusion model, which achieved a more accurate prediction of brain age (MAE, 3.96 years; r = .76, p <.001). Notably, the fusion model achieved better improvement in the group of older subjects (70-85 years). Extracted attention maps of the network showed that amygdala, pallidum, and olfactory were effective for age estimation. Mediation analysis further showed that brain structural features and blood parameters provided independent and significant impact. The constructed age prediction model may have promising potential in evaluation of brain health based on MRI and blood parameters.

Transmission in home environment associated with the second wave of COVID-19 pandemic in India.

India has suffered from the second wave of COVID-19 pandemic since March 2021. This wave of the outbreak has been more serious than the first wave pandemic in 2020, which suggests that some new transmission characteristics may exist. COVID-19 is transmitted through droplets, aerosols, and contact with infected surfaces. Air pollutants are also considered to be associated with COVID-19 transmission. However, the roles of indoor transmission in the COVID-19 pandemic and the effects of these factors in indoor environments are still poorly understood. Our study focused on reveal the role of indoor transmission in the second wave of COVID-19 pandemic in India. Our results indicated that human mobility in the home environment had the highest relative influence on COVID-19 daily growth rate in the country. The COVID-19 daily growth rate was significantly positively correlated with the residential percent rate in most state-level areas in India. A significant positive nonlinear relationship was found when the residential percent ratio ranged from 100 to 120%. Further, epidemic dynamics modelling indicated that a higher proportion of indoor transmission in the home environment was able to intensify the severity of the second wave of COVID-19 pandemic in India. Our findings suggested that more attention should be paid to the indoor transmission in home environment. The public health strategies to reduce indoor transmission such as ventilation and centralized isolation will be beneficial to the prevention and control of COVID-19.

Biomimetic mineralisation systems for in situ enamel restoration inspired by amelogenesis.

Caries and dental erosion are common oral diseases. Traditional treatments involve the mechanical removal of decay and filling but these methods are not suitable for cases involving large-scale enamel erosion, such as hypoplasia. To develop a noninvasive treatment, promoting remineralisation in the early stage of caries is of considerable clinical significance. Therefore, biomimetic mineralisation is an ideal approach for restoring enamel. Biomimetic mineralisation forms a new mineral layer that is tightly attached to the surface of the enamel. This review details the state-of-art achievements on the application of amelogenin and non-amelogenin, amorphous calcium phosphate, ions flow and other techniques in the biomimetic mineralisation of enamel. The ultimate goal of this review was to shed light on the requirements for enamel biomineralisation. Hence, herein, we summarise two strategies of biological minimisation systems for in situ enamel restoration inspired by amelogenesis that have been developed in recent years and compare their advantages and disadvantages.

Selenoprotein F knockout leads to glucose and lipid metabolism disorders in mice.

Selenoprotein F (Selenof), an endoplasmic reticulum (ER)-resident protein, is considered to be involved in glycoprotein folding and quality control in the ER. However, its function has not yet been thoroughly addressed. In this study, proteomics analysis revealed that Selenof deficiency in mice led to the differential expression of hepatic proteins associated with glucose and lipid metabolism. The phenotype analysis revealed that Selenof knockout mice showed glucose intolerance and insulin reduction, even with a normal diet. Additionally, Selenof knockout exacerbated high-fat diet-induced obesity, hyperglycemia, glucose intolerance, and hepatic steatosis. Furthermore, lipoprotein lipase and carboxylesterase 1D, two glycoproteins involved in lipid metabolism, were significantly decreased in the liver of Selenof knockout mice with a normal or high-fat diet. Collectively, these findings suggested that Selenof deficiency might cause the perturbation of glycoprotein quality control and thus contribute to glucose and lipid metabolism disorders, implying a novel biological function of Selenof.

Distinct Functions of Endophilin Isoforms in Synaptic Vesicle Endocytosis.

Endophilin isoforms perform distinct characteristics in their interactions with N-type Ca(2+) channels and dynamin. However, precise functional differences for the endophilin isoforms on synaptic vesicle (SV) endocytosis remain unknown. By coupling RNA interference and electrophysiological recording techniques in cultured rat hippocampal neurons, we investigated the functional differences of three isoforms of endophilin in SV endocytosis. The results showed that the amplitude of normalized evoked excitatory postsynaptic currents in endophilin1 knockdown neurons decreased significantly for both single train and multiple train stimulations. Similar results were found using endophilin2 knockdown neurons, whereas endophilin3 siRNA exhibited no change compared with control neurons. Endophilin1 and endophilin2 affected SV endocytosis, but the effect of endophilin1 and endophilin2 double knockdown was not different from that of either knockdown alone. This result suggested that endophilin1 and endophilin2 functioned together but not independently during SV endocytosis. Taken together, our results indicate that SV endocytosis is sustained by endophilin1 and endophilin2 isoforms, but not by endophilin3, in primary cultured hippocampal neurons.

Selenoprotein W modulates tau homeostasis in an Alzheimer's disease mouse model.

Lower selenium levels are observed in Alzheimer's disease (AD) brains, while supplementation shows multiple benefits. Selenoprotein W (SELENOW) is sensitive to selenium changes and binds to tau, reducing tau accumulation. However, whether restoration of SELENOW has any protective effect in AD models and its underlying mechanism remain unknown. Here, we confirm the association between SELENOW downregulation and tau pathology, revealing SELENOW's role in promoting tau degradation through the ubiquitin‒proteasome system. SELENOW competes with Hsp70 to interact with tau, promoting its ubiquitination and inhibiting tau acetylation at K281. SELENOW deficiency leads to synaptic defects, tau dysregulation and impaired long-term potentiation, resulting in memory deficits in mice. Conversely, SELENOW overexpression in the triple transgenic AD mice ameliorates memory impairment and tau-related pathologies, featuring decreased 4-repeat tau isoform, phosphorylation at Ser396 and Ser404, neurofibrillary tangles and neuroinflammation. Thus, SELENOW contributes to the regulation of tau homeostasis and synaptic maintenance, implicating its potential role in AD.

Comparative Proteomic Analysis Reveals the Effect of Selenoprotein W Deficiency on Oligodendrogenesis in Fear Memory.

The essential trace element selenium plays an important role in maintaining brain function. Selenoprotein W (SELENOW), the smallest selenoprotein that has been identified in mammals, is sensitive to selenium levels and abundantly expressed in the brain. However, its biological role in the brain remains to be clarified. Here, we studied the morphological and functional changes in the brain caused by SELENOW deficiency using its gene knockout (KO) mouse models. Histomorphological alterations of the amygdala and hippocampus, specifically in the female SELENOW KO mice, were observed, ultimately resulting in less anxiety-like behavior and impaired contextual fear memory. Fear conditioning (FC) provokes rapidly intricate responses involving neuroplasticity and oligodendrogenesis. During this process, the females generally show stronger contextual FC than males. To characterize the effect of SELENOW deletion on FC, specifically in the female mice, a Tandem mass tag (TMT)-based comparative proteomic approach was applied. Notably, compared to the wildtype (WT) no shock (NS) mice, the female SELENOW KO NS mice shared lots of common differentially expressed proteins (DEPs) with the WT FC mice in the hippocampus, enriched in the biological process of ensheathment and oligodendrocyte differentiation. Immunostaining and Western blotting analyses further confirmed the proteomic results. Our work may provide a holistic perspective of gender-specific SELENOW function in the brain and highlighted its role in oligodendrogenesis during fear memory.

An Adequate Supply of Bis(ethylmaltolato)oxidovanadium(IV) Remarkably Reversed the Pathological Hallmarks of Alzheimer's Disease in Triple-Transgenic Middle-Aged Mice.

Alzheimer's disease (AD) is a complex and progressive neurodegenerative disease with impaired synapse, imbalanced mineral metabolism, protein mis-folding and aggregation. Bis(ethylmaltolato)oxidovanadium(IV) (BEOV), an organic bioactive vanadium compound with low toxicity and high bioavailability, has been studied as therapeutic agent against tuberculosis and diabetes. However, its neuroprotective effects have rarely been reported. Therefore, in this study, the potential application of BEOV in intervening AD cognitive dysfunction and neuropathology was evaluated. Both low- and high-dose of BEOV (0.2 mmol/L and 1.0 mmol/L) supplementation for 2 months improved the spatial learning and memory deficits of the triple-transgenic AD (3 × Tg AD) mice and mitigated the loss of synaptic proteins and synaptic dysfunction. By inhibiting the expression of amyloid-ß precursor protein and ß-secretase, and the phosphorylation of tau protein at Ser262, Ser396, Ser404, and Ser202/Thr205 residues, BEOV reduced the amyloid-ß deposition and neurofibrillary tangle formation in AD mouse brains and primarily cultured neurons. Further analysis of the brain ionome revealed that BEOV supplementation could significantly affect the concentrations of a variety of metals, most of which, including several AD risk metals, showed reduced levels, particularly with a high-dose intake. Additionally, the elemental correlation network identified both conserved and specific elemental correlations, implying a highly complex and dynamic crosstalk between vanadium and other elements during long-term BEOV supplementation. Overall, our results suggest that BEOV is effective in AD intervention via both ameliorating the disease related pathology and regulating metal homeostasis.

Sunlight ultraviolet radiation dose is negatively correlated with the percent positive of SARS-CoV-2 and four other common human coronaviruses in the U.S.

Human coronaviruses are RNA viruses that are sensitive to ultraviolet (UV) radiation. Sunlight contains UVA (320-400 nm), UVB (260-320 nm) and UVC (200-260 nm) action spectra. UVC can inactivate coronaviruses, including severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2). The incidence and mortality of coronavirus disease 2019 (COVID-19) are considered to be correlated with vitamin D levels. Vitamin D synthesis in human skin is closely related to exposure to UVB radiation. Therefore, the incidence and mortality of COVID-19 are also considered to be correlated with Vitamin D levels. In this study, Spearman and Kendall rank correlation analysis tests were used to analyze the correlation between the average percent positive of five human coronaviruses (SARS-CoV-2, CoVHKU1, CoVNL63, CoVOC43, and CoV229E) in the U.S. and the corresponding sunlight UV radiation dose The results indicated that the monthly average percent positive of four common coronaviruses was significantly negatively correlated with the sunlight UV radiation dose. The weekly percent positive of SARS-CoV-2 during April 17, 2020 to July 10, 2020 showed a significant negative correlation with the sunlight UV radiation dose in census regions 1 and 2 of the U.S. while no statistical significance in the other regions. Additionally, sunlight UV radiation also showed some negative effects with respect to the early SARS-CoV-2 transmission.

Bis(ethylmaltolato)oxidovanadium (IV) attenuates amyloid-beta-mediated neuroinflammation by inhibiting NF-κB signaling pathway via a PPARγ-dependent mechanism.

Neuroinflammation plays a pivotal role in the pathophysiology of neurodegenerative diseases, such as Parkinson's disease and Alzheimer's disease. During brain neuroinflammation, activated microglial cells resulting from amyloid-beta (Aß) overload trigger toxic proinflammatory responses. Bis(ethylmaltolato)oxidovanadium (BEOV) (IV), an important vanadium compound, has been reported to have anti-diabetic, anti-cancer, and neuroprotective effects, but its anti-inflammatory property has rarely been investigated. In the present study, the inhibitory effects of BEOV on neuroinflammation were revealed in both Aß-stimulated BV2 microglial cell line and APPswe/PS1E9 transgenic mouse brain. BEOV administration significantly decreased the levels of tumor necrosis factor-α, interleukin-6, interleukin-1ß, inducible nitric oxide synthase, and cyclooxygenase-2 both in the hippocampus of APPswe/PS1E9 mice and in the Aß-stimulated BV2 microglia. Furthermore, BEOV suppressed the Aß-induced activation of nuclear factor-κB (NF-κB) signaling and upregulated the protein expression level of peroxisome proliferator-activated receptor gamma (PPARγ) in a dose-dependent manner. PPARγ inhibitor GW9662 could eliminate the effect of BEOV on Aß-induced NF-κB activation and proinflammatory mediator production. Taken altogether, these findings suggested that BEOV ameliorates Aß-stimulated neuroinflammation by inhibiting NF-κB signaling pathway through a PPARγ-dependent mechanism.

An electrochemical aptasensor based on AuPt alloy nanoparticles for ultrasensitive detection of amyloid-ß oligomers.

Amyloid-ß oligomer is an important biomarker and a potential therapeutic target of Alzheimer's disease in its early stage. Here, we combined superhydrophobic carbon fiber paper (CFP) with AuPt alloy nanoparticles to prepare a CFP/AuPt nanocomposite with larger specific surface area and hydrophobic surface. On this basis, we constructed an electrochemical aptasensor based on CFP/AuPt for the ultrasensitive detection of amyloid-ß oligomers. The surface-coated AuPt nanoparticles greatly enhanced the electroactive area, and the hydrophobic surface increased the resisting nonspecific adsorption performance of sensor. A combination of these two features significantly improved the sensitivity and specificity of the sensor. This electrochemical aptasensor based on CFP/AuPt displayed a low detection limit of 0.16 pg/mL. This work shows a promising future in clinical diagnosis of Alzheimer's disease and provides a possible solution to electrochemical biosensors that are susceptible to interference in biological fluids.

Bis(ethylmaltolato)oxidovanadium (IV) mitigates neuronal apoptosis resulted from amyloid-beta induced endoplasmic reticulum stress through activating peroxisome proliferator-activated receptor γ.

Neuronal apoptosis caused by amyloid-beta (Aß) overproduction is one of the most important pathological features in Alzheimer's disease (AD). Endoplasmic reticulum (ER) stress induced by Aß overload plays a critical role in this process. Bis(ethylmaltolato)oxidovanadium (IV) (BEOV), a vanadium compound which had been regarded as peroxisome proliferator-activated receptor γ (PPARγ) agonist, was reported to exert an antagonistic effect on ER stress. In this study, we tested whether BEOV could ameliorate the Aß-induced neuronal apoptosis by inhibiting ER stress. It was observed that BEOV treatment ameliorated both tunicamycin-induced and/or Aß-induced ER stress and neurotoxicity in a dose-dependent manner through downgrading ER stress-associated and apoptosis-associated proteins in primary hippocampal neurons. Consistent with in vitro results, BEOV also reduced ER stress and inhibited neuronal apoptosis in hippocampi and cortexes of transgenic AD model mice. Moreover, by adopting GW9662 and salubrinal, the inhibitor of PPARγ and hyperphosphorylated eukaryotic translation initiation factor 2α, respectively, we further confirmed that BEOV alleviated Aß-induced ER stress and neuronal apoptosis in primary hippocampal neurons by activating PPARγ. Taken together, these results provided scientific evidences to support the concept that BEOV ameliorates Aß-induced ER stress and neuronal apoptosis through activating PPARγ.

Hepatic proteomic analysis of selenoprotein F knockout mice by iTRAQ: An implication for the roles of selenoprotein F in metabolism and diseases.

Selenoprotein F (Selenof) is an endoplasmic reticulum (ER)-resident protein. It may be functionally linked to glycoprotein folding in the ER but the detail function is not fully understood. To study the function of Selenof, we used CRISPR/Cas9 to generate Selenof knockout mice and performed proteomic analysis of hepatic proteins by iTRAQ. Collectively, 83 differently expressed proteins (DEPs) were identified in the liver of Selenof knockout mice. The changes of mRNA and protein levels of 6 selected DEPs, Fatty acid synthase, ATP-citrate synthase, Glutathione S-transferase P 1, Transformer-2 protein homolog beta, Pyruvate kinase, Metallothionein-2, were further verified by quantitative real-time PCR or Western blot. The roles of 83 DEPs are mainly related to metabolism and cancer. Consistently, the levels of NADPH and ATP, two molecules closely related to energy metabolism, are significantly changed in the livers of Selenof knockout mice. SIGNIFICANCE: Our study identified potential biological pathways and proteins related to Selenof deletion. These findings will provide possible proteins/pathways related to Selenof and help to understand the function of Selenof as well as the relationship between Selenof and certain diseases.

Transcriptional Regulation of Selenoprotein F by Heat Shock Factor 1 during Selenium Supplementation and Stress Response.

Changes of Selenoprotein F (SELENOF) protein levels have been reported during selenium supplementation, stressful, and pathological conditions. However, the mechanisms of how these external factors regulate SELENOF gene expression are largely unknown. In this study, HEK293T cells were chosen as an in vitro model. The 5'-flanking regions of SELENOF were analyzed for promoter features. Dual-Glo Luciferase assays were used to detect promoter activities. Putative binding sites of Heat Shock Factor 1 (HSF1) were predicted in silico and the associations were further proved by chromatin immunoprecipitation (ChIP) assay. Selenate and tunicamycin (Tm) treatment were used to induce SELENOF up-regulation. The fold changes in SELENOF expression and other relative proteins were analyzed by Q-PCR and western blot. Our results showed that selenate and Tm treatment up-regulated SELENOF at mRNA and protein levels. SELENOF 5'-flanking regions from -818 to -248 were identified as core positive regulatory element regions. Four putative HSF1 binding sites were predicted in regions from -1430 to -248, and six out of seven primers detected positive results in ChIP assay. HSF1 over-expression and heat shock activation increased the promoter activities, and mRNA and protein levels of SELENOF. Over-expression and knockdown of HSF1 showed transcriptional regulation effects on SELENOF during selenate and Tm treatment. In conclusion, HSF1 was discovered as one of the transcription factors that were associated with SELENOF 5'-flanking regions and mediated the up-regulation of SELENOF during selenate and Tm treatment. Our work has provided experimental data for the molecular mechanism of SELENOF gene regulation, as well as uncovered the involvement of HSF1 in selenotranscriptomic for the first time.

Role of Selenoprotein F in Protein Folding and Secretion: Potential Involvement in Human Disease.

Selenoproteins form a group of proteins of which its members contain at least one selenocysteine, and most of them serve oxidoreductase functions. Selenoprotein F (SELENOF), one of the 25 currently identified selenoproteins, is located in the endoplasmic reticulum (ER) organelle and is abundantly expressed in many tissues. It is regulated according to its selenium status, as well as by cell stress conditions. SELENOF may be functionally linked to protein folding and the secretion process in the ER. Several studies have reported positive associations between SELENOF genetic variations and several types of cancer. Also, altered expression levels of SELENOF have been found in cancer cases and neurodegenerative diseases. In this review, we summarize the current understanding of the structure, expression, and potential function of SELENOF and discuss its possible relation with various pathological processes.

Comparative proteomics reveals the neurotoxicity mechanism of ER stressors tunicamycin and dithiothreitol.

Severity or duration of endoplasmic reticulum (ER) stress leads to two different cellular events: cell survival and apoptosis. Drug-induced ER stress or neurotoxicity has been observed as one of the main side effects. However, how ER stress affects cellular signaling cascades leading to neuronal damage is still not well understood. In this study, the toxicological mechanisms of two typical ER stress inducers, tunicamycin (Tm) and dithiothreitol (DTT), were investigated by cell viability, unfolded protein response, apoptosis and proteomic responses in mouse neuro-2a cells. A large portion of differentially expressed proteins (DEPs) that participate in protein synthesis and folding were identified in the Tm treated group, indicating adaptive cellular responses like the unfolded protein response were activated, which was not the case in the DTT treated group. Interestingly, KEGG pathway analysis and validation experiments revealed that proteins involved in proteasomal degradation were down-regulated by both inducers, while proteins involved in ubiquitination were up-regulated by Tm and down-regulated by DTT. A protein responsible for delivering ubiquitinated proteins to the proteasome, the UV excision repair protein RAD23 homolog A (HR23 A), was discovered as a DEP altered by both Tm and DTT. This protein was down-regulated in the Tm treated group and up-regulated in the DTT treated group, which explained the differences we observed in the ubquintination and proteasomal degradation pathways. Autophagy was activated in the Tm treated group, suggesting that it may serve as a compensatory effect to proteasomal degradation. Our work provides new insights into the neurotoxicity generated by various ER stress inducers and the underlying mechanisms.

PDLIM5 mediates PKCε translocation in PMA-induced growth cone collapse.

Growth cone collapse is a critical repulsive response to various guidance cues for axon guidance. Protein kinase C epsilon (PKCε) plays important regulation roles in such responses. Translocation of PKCε from cytoplasm to membrane is crucial to archive its regulatory roles in this process. We previously reported that PDLIM5 could selectively recruit PKCε to its specific substrate in neurons. However, the molecular mechanism of PKCε translocation in the neuronal growth cone collapse remains elusive. Here, we demonstrated that PDLIM5 and PKCε co-existed in the nerve growth cones. By interacting with α-actinin, but not ß-actin or ß-tubulin, PDLIM5 might contribute to regulation of remodeling of the microfilaments in neurons. Meanwhile, PDLIM5 could also bind to PKCε to form PDLIM5-PKCε complexes in growth cones. In the primary cultured neurons, activation of PKCε by PMA resulted in translocation of both PKCε and PDLIM5 from cytoplasm to the membrane. Knockdown of either PDLIM5 or PKCε rescued the neuron from PMA-induced growth cone collapse. Furthermore, in neurons, application of PDLIM5 shRNA or over-expression of PDLIM5 LIM1-3 mutants reduced the amount of PKCε in the membrane. Together, these results suggest that PDLIM5 acts as a scaffold protein by mediated PKCε translocated to the membrane in PMA-induced growth cone collapse.