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Supplementary Materials and Methods

One-carbon (1C) metabolism has a key role in metabolic programming with both mitochondrial (m1C) and cytoplasmic (c1C) components. Here we show that activating transcription factor 4 (ATF4) exclusively activates gene expression involved in m1C, but not the c1C cycle in prostate cancer cells. This includes activation of methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) expression, the central player in the m1C cycle. Consistent with the key role of m1C cycle in prostate cancer, MTHFD2 knockdown inhibited prostate cancer cell growth, prostatosphere formation, and growth of patient-derived xenograft organoids. In addition, therapeutic silencing of MTHFD2 by systemically administered nanoliposomal siRNA profoundly inhibited tumor growth in preclinical prostate cancer mouse models. Consistently, MTHFD2 expression is significantly increased in human prostate cancer, and a gene expression signature based on the m1C cycle has significant prognostic value. Furthermore, MTHFD2 expression is coordinately regulated by ATF4 and the oncoprotein c-MYC, which has been implicated in prostate cancer. These data suggest that the m1C cycle is essential for prostate cancer progression and may serve as a novel biomarker and therapeutic target.Significance:These findings demonstrate that the mitochondrial, but not cytoplasmic, one-carbon cycle has a key role in prostate cancer cell growth and survival and may serve as a biomarker and/or therapeutic target.

Chimeric antigen receptors (CARs) that retarget T cells against CD19 show clinical efficacy against B cell malignancies. Here, we describe the development of a CAR against the six-transmembrane epithelial antigen of prostate-1 (STEAP1), which is expressed in ∼90% of prostate cancers, and subgroups of other malignancies. STEAP1 is an attractive target, as it is associated with tumor invasiveness and progression and only expressed at low levels in normal tissues, apart from the non-vital prostate gland. We identified the antibody coding sequences from a hybridoma and designed a CAR that is efficiently expressed in primary T cells. The T cells acquired the desired anti-STEAP1 specificity, with a polyfunctional response including production of multiple cytokines, proliferation, and the killing of cancer cells. The response was observed for both CD4

One-carbon (1C) metabolism has a key role in metabolic programming with both mitochondrial (m1C) and cytoplasmic (c1C) components. Here we show that activating transcription factor 4 (ATF4) exclusively activates gene expression involved in m1C, but not the c1C cycle in prostate cancer cells. This includes activation of methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) expression, the central player in the m1C cycle. Consistent with the key role of m1C cycle in prostate cancer, MTHFD2 knockdown inhibited prostate cancer cell growth, prostatosphere formation, and growth of patient-derived xenograft organoids. In addition, therapeutic silencing of MTHFD2 by systemically administered nanoliposomal siRNA profoundly inhibited tumor growth in preclinical prostate cancer mouse models. Consistently, MTHFD2 expression is significantly increased in human prostate cancer, and a gene expression signature based on the m1C cycle has significant prognostic value. Furthermore, MTHFD2 expression is coordinately regulated by ATF4 and the oncoprotein c-MYC, which has been implicated in prostate cancer. These data suggest that the m1C cycle is essential for prostate cancer progression and may serve as a novel biomarker and therapeutic target. Significance: These findings demonstrate that the mitochondrial, but not cytoplasmic, one-carbon cycle has a key role in prostate cancer cell growth and survival and may serve as a biomarker and/or therapeutic target.

Cardiac myosin binding protein C (cMyBP-C) is a phosphorylation-dependent force regulator and plays an important role in controlling myosin and actin dynamic interaction. Point-mutations of cMyBP-C that interfere with cMyBP-C threonine/serine phosphorylation resulted in hypertrophic cardiomyopathy and cardiac failure. However, it remains largely unknown how cMyBP-C tyrosine phosphorylation is regulated during cardiac hypertrophy and heart failure. Integrins are receptors of extracellular matrix and are the sensors of cardiac mechanical stretch. Focal adhesion kinase (FAK) plays an essential role in integrin-initiated signal transduction and regulates multiple cellular functions in various types of cells including cardiomyocytes. To identify the regulatory mechanism of cMyBP-C tyrosine phosphorylation during cardiac hypertrophy, we examined the effect of FAK on phosphorylation of cMyBP-C. Immunoprecipitation analysis showed that FAK and cMyBP-C are associated within the intact mouse heart. Results from our mutagenesis experiments demonstrated that the FAK kinase domain was required for FAK to associate with cMyBP-C. Our data also documented that the FAK Y397 site is required for FAK and cMyBP-C association. Importantly, overexpression dominant active Src Y527F with FAK significantly enhanced cMyBP-C phosphorylation. Interestingly, overexpression of cMyBP-C inhibited FAK phosphorylation. Taken together, cMyBP-C is one of effectors of Src/FAK complex in cardiomyocyte.

Cdc42, a Ras-related GTPase that regulates the actin cytoskeleton, was recently shown to play an indispensable role in vasculogenesis and endothelial cell (EC) survival. Here, we determined whether Cdc42 also contributes to lymphatic development by generated two different Cdc42 knockout mice lines by crossing Cdc42/flox mice with either vascular endothelial cadherin-Cre (Cdh5α-Cre) mice or Prox1-CreERT2 mice. Our results demonstrated that depleting ECs of Cdc42 expression resulted in embryonic lethality with severe edema. Whole-mount immunofluorescence staining of both knockout embryos showed that the deletion of Cdc42 in ECs impaired lymphatic vessel branching and that the lymphatic lumen size significantly increased. Moreover, we found that the inactivation of Cdc42 compromised mesenteric collecting lymphatic vessel maturation and prevented valve formation. We go on to show that Cdc42 can be activated by vascular endothelial growth factor c (VEGFc) in cultured human dermal lymphatic ECs (HDLECs), and that knocking down Cdc42 expression in these cells using siRNA decreased VEGFc-induced focal adhesion kinase (FAK) phosphorylation. These findings, when taken together with the fact that inactivating FAK plus one allele of Cdc42 in ECs was sufficient to recapitulate the phenotypes of the Cdc42 EC knockout embryos, suggests that Cdc42 and FAK interact genetically during lymphatic development. In addition, Cdc42 and FAK regulated signal transduction is essential for blood and lymphatic vessel separation. Taken together, our data highlights the important role played by Cdc42 in the development of the lymphatic system.

In this work, the kinetics of transformation of iodide (I–) and hypoiodous acid (HOI) by peroxymonosulfate (PMS) and potential formation of worrisome iodinated products in the presence of natural organic matter (NOM) were investigated. As the pH increased from 5 to 10, the apparent second-order rate constants of reaction of PMS with I– gradually decreased from 1.01 × 103 to 3.86 × 102 M–1 s–1, while those for HOI increased dramatically from 1.08 × 102 to 7.90 × 104 M–1 s–1. The obtained pH-dependent rate profiles were explained well by the effects of pH-affected speciation of PMS and/or HOI. Considerable amounts of total organic iodine (TOI) could be formed in the PMS/I–/NOM system over a wide pH range. Under similar conditions, the TOI levels formed in the PMS/I–/NOM system were generally higher than those formed in the case of HOCl but much lower than those formed in the case of NH2Cl. Also, specific iodoform (IF) and monoiodoacetic acid (MIAA) were detected in both simulated and authentic waters during...

In this study, we interestingly found that peroxydisulfate (PDS) could be activated by a commercial multiwalled carbon nanotube (CNT) material via a nonradical pathway. Iodide (I–) was quickly and almost completely oxidized to hypoiodous acid (HOI) in the PDS/CNT system over the pH range of 5–9, but the further transformation to iodate (IO3–) was negligible. A kinetic model was proposed, which involved the formation of reactive PDS-CNT complexes, and then their decomposition into sulfate anion (SO42–) via inner electron transfer within the complexes or by competitively reacting with I–. Several influencing factors (e.g., PDS and CNT dosages, and solution pH) on I– oxidation kinetics by this system were evaluated. Humic acid (HA) decreased the oxidation kinetics of I–, probably resulting from its inhibitory effect on the interaction between PDS and CNT to form the reactive complexes. Moreover, adsordable organic iodine compounds (AOI) as well as specific iodoform and iodoacetic acid were appreciably produc...

Cancer cells exploit many of the cellular adaptive responses to support their survival needs. One such critical pathway in eukaryotic cells is the unfolded protein response (UPR) that is important in normal physiology as well as disease states, including cancer. Since UPR can serve as a lever between survival and death, regulated control of its activity is critical for tumor formation and growth although the underlying mechanisms are poorly understood. Here we show that one of the main transcriptional effectors of UPR, activating transcription factor 4 (ATF4), is essential for prostate cancer (PCa) growth and survival. Using systemic unbiased gene expression and proteomic analyses, we identified a novel direct ATF4 target gene, family with sequence similarity 129 member A (FAM129A), which is critical in mediating ATF4 effects on prostate tumorigenesis. Interestingly, FAM129A regulated both PERK and eIF2a in a feedback loop that differentially channeled the UPR output. ATF4 and FAM129A protein expression is increased in patient PCa samples compared with benign prostate. Importantly, in vivo therapeutic silencing of ATF4-FAM129A axis profoundly inhibited tumor growth in a preclinical PCa model. These data support that one of the canonical UPR branches, through ATF4 and its target gene FAM129A, is required for PCa growth and thus may serve as a novel therapeutic target.

The transformation efficiency and products of an odorous compound 2,4,6-trichloroanisole (TCA) at the wavelength of 254 nm in the presence of persulfate were investigated for the first time. The effects of water matrix (i.e., natural organic matter (NOM), pH, carbonate/bicarbonate (HCO3(-)/CO3(2-)), and chloride ions (Cl(-))) were evaluated. The second order rate constant of TCA reacting with sulfate radical (SO4(-)) was determined to be (3.72 ± 0.10) × 10(9) M(-1) s(-1). Increasing dosage of persulfate increased the observed pseudo-first-order rate constant for TCA degradation (kobs), and the contribution of SO4(-) to TCA degradation was much higher than that of HO at each experimental condition. Degradation rate of TCA decreased with pH increasing from 4.0 to 9.0, which could be explained by the lower radical scavenging effect of dihydrogen phosphate than hydrogen phosphate in acidic condition (pH

Deep neural networks can model images with rich latent representations, but they cannot naturally conceptualize structures of object categories in a human-perceptible way. This paper addresses the problem of learning object structures in an image modeling process without supervision. We propose an autoencoding formulation to discover landmarks as explicit structural representations. The encoding module outputs landmark coordinates, whose validity is ensured by constraints that reflect the necessary properties for landmarks. The decoding module takes the landmarks as a part of the learnable input representations in an end-to-end differentiable framework. Our discovered landmarks are semantically meaningful and more predictive of manually annotated landmarks than those discovered by previous methods. The coordinates of our landmarks are also complementary features to pretrained deep-neural-network representations in recognizing visual attributes. In addition, the proposed method naturally creates an unsupervised, perceptible interface to manipulate object shapes and decode images with controllable structures. The project webpage is at http://ytzhang.net/projects/lmdis-rep, Comment: 48 pages

The presence of acetic acid during industrial alcohol fermentation reduces the yield of fermentation by imposing additional stress on the yeast cells. The biology of cellular responses to stress has been a subject of vigorous investigations. Although much has been learned, details of some of these responses remain poorly understood. Members of heat shock chaperone HSP proteins have been linked to acetic acid and heat shock stress responses in yeast. Both acetic acid and heat shock have been identified to trigger different cellular responses including reduction of global protein synthesis and induction of programmed cell death. Yeast HSC82 and HSP82 code for two important heat shock proteins that together account for 1-2% of total cellular proteins. Both proteins have been linked to responses to acetic acid and heat shock. In contrast to the overall rate of protein synthesis which is reduced, the expression of HSC82 and HSP82 is induced in response to acetic acid stress. In the current study we identified two yeast genes DOM34 and RPL36A that are linked to acetic acid and heat shock sensitivity. We investigated the influence of these genes on the expression of HSP proteins. Our observations suggest that Dom34 and RPL36A influence translation in a CAP-independent manner., This work was funded by the Natural Sciences and Engineering Research Council of Canada, NSERC., info:eu-repo/semantics/publishedVersion

Neural crest cells (NCCs) are physically responsible for craniofacial skeleton formation, pharyngeal arch artery remodeling and cardiac outflow tract septation during vertebrate development. Cdc42 (cell division cycle 42) is a Rho family small GTP-binding protein that works as a molecular switch to regulate cytoskeleton remodeling and the establishment of cell polarity. To investigate the role of Cdc42 in NCCs during embryonic development, we deleted Cdc42 in NCCs by crossing Cdc42 flox mice with Wnt1-cre mice. We found that the inactivation of Cdc42 in NCCs caused embryonic lethality with craniofacial deformities and cardiovascular developmental defects. Specifically, Cdc42 NCC knockout embryos showed fully penetrant cleft lips and short snouts. Alcian Blue and Alizarin Red staining of the cranium exhibited an unfused nasal capsule and palatine in the mutant embryos. India ink intracardiac injection analysis displayed a spectrum of cardiovascular developmental defects, including persistent truncus arteriosus, hypomorphic pulmonary arteries, interrupted aortic arches, and right-sided aortic arches. To explore the underlying mechanisms of Cdc42 in the formation of the great blood vessels, we generated Wnt1Cre-Cdc42-Rosa26 reporter mice. By beta-galactosidase staining, a subpopulation of Cdc42-null NCCs was observed halting in their migration midway from the pharyngeal arches to the conotruncal cushions. Phalloidin staining revealed dispersed, shorter and disoriented stress fibers in Cdc42-null NCCs. Finally, we demonstrated that the inactivation of Cdc42 in NCCs impaired bone morphogenetic protein 2 (BMP2)-induced NCC cytoskeleton remodeling and migration. In summary, our results demonstrate that Cdc42 plays an essential role in NCC migration, and inactivation of Cdc42 in NCCs impairs craniofacial and cardiovascular development in mice.

Cdc42 is a member of the Rho GTPase family and functions as a molecular switch in regulating cell migration, proliferation, differentiation and survival. However, the role of Cdc42 in heart development remains largely unknown. To determine the function of Cdc42 in heart formation, we have generated a Cdc42 cardiomyocyte knockout (CCKO) mouse line by crossing Cdc42 flox mice with myosin light chain (MLC) 2a-Cre mice. The inactivation of Cdc42 in embryonic cardiomyocytes induced lethality after embryonic day 12.5. Histological analysis of CCKO embryos showed cardiac developmental defects that included thin ventricular walls and ventricular septum defects. Microarray and real-time PCR data also revealed that the expression level of p21 was significantly increased and cyclin B1 was dramatically decreased, suggesting that Cdc42 is required for cardiomyocyte proliferation. Phosphorylated Histone H3 staining confirmed that the inactivation of Cdc42 inhibited cardiomyocytes proliferation. In addition, transmission electron microscope studies showed disorganized sarcomere structure and disruption of cell-cell contact among cardiomyocytes in CCKO hearts. Accordingly, we found that the distribution of N-cadherin/β-Catenin in CCKO cardiomyocytes was impaired. Taken together, our data indicate that Cdc42 is essential for cardiomyocyte proliferation, sarcomere organization and cell-cell adhesion during heart development.

Fibroblast growth factor 1 (FGF1) taken up by cells into endocytic vesicles can be translocated across vesicular membranes into the cytosol and the nucleus where it has a growth regulatory activity. Previously, leucine-rich repeat containing 59 (LRRC59) was identified as an intracellular binding partner of FGF1, but its biological role remained unknown. Here, we show that LRRC59 is strictly required for nuclear import of exogenous FGF1. siRNA-mediated depletion of LRRC59 did not inhibit the translocation of FGF1 into cytosol, but blocked the nuclear import of FGF1. We also found that an nuclear localization sequence (NLS) in FGF1, Ran GTPase, karyopherin-α1 (Kpnα1), and Kpnβ1 were required for nuclear import of FGF1. Nuclear import of exogenous FGF2, which depends on CEP57/Translokin, was independent of LRRC59, but was dependent on Kpnα1 and Kpnβ1, while the nuclear import of FGF1 was independent of CEP57. LRRC59 is a membrane-anchored protein that localizes to the endoplasmic reticulum (ER) and the nuclear envelope (NE). We found that LRRC59 possesses NLS-like sequences in its cytosolic part that can mediate nuclear import of soluble LRRC59 variants, and that the localization of LRRC59 to the NE depends on Kpnβ1. We propose that LRRC59 facilitates transport of cytosolic FGF1 through nuclear pores by interaction with Kpns and movement of LRRC59 along the ER and NE membranes.

Cdc42 is a member of the Rho GTPase family and functions as a molecular switch in regulating cell migration, proliferation, differentiation and survival. However, the role of Cdc42 in heart development remains largely unknown. To determine the function of Cdc42 in heart formation, we have generated a Cdc42 cardiomyocyte knockout (CCKO) mouse line by crossing Cdc42 flox mice with myosin light chain (MLC) 2a-Cre mice. The inactivation of Cdc42 in embryonic cardiomyocytes induced lethality after embryonic day 12.5. Histological analysis of CCKO embryos showed cardiac developmental defects that included thin ventricular walls and ventricular septum defects. Microarray and real-time PCR data also revealed that the expression level of p21 was significantly increased and cyclin B1 was dramatically decreased, suggesting that Cdc42 is required for cardiomyocyte proliferation. Phosphorylated Histone H3 staining confirmed that the inactivation of Cdc42 inhibited cardiomyocytes proliferation. In addition, transmission electron microscope studies showed disorganized sarcomere structure and disruption of cell-cell contact among cardiomyocytes in CCKO hearts. Accordingly, we found that the distribution of N-cadherin/β-Catenin in CCKO cardiomyocytes was impaired. Taken together, our data indicate that Cdc42 is essential for cardiomyocyte proliferation, sarcomere organization and cell-cell adhesion during heart development.

Cdc42 is a Ras-related GTPase that plays an important role in regulation of actin cytoskeletal architecture. Blocking the ability of Cdc42 to activate its effectors has been shown to inhibit a range of cellular functions including cell polarization, migration, proliferation and differentiation. Consistent with its critical roles in vitro, the inactivation of Cdc42 in mice resulted in embryonic lethality before E6.5. The early embryonic lethal phenotype of Cdc42-null mice has made it not useful for studies on the interesting questions of the roles and mechanisms of Cdc42 in the vascular development. To overcome this problem, we have generated an endothelial cell (EC) specific Cdc42 knockout mouse line by crossing Cdc42/flox mice with vascular endothelial cadherin Cre mice. Our results have demonstrated that the deletion of Cdc42 in ECs resulted in embryonic lethality with severe edema. Whole mount immunofluorescence staining showed mesentery collecting lymphatic vessel maturation and valve formation defects. Interestingly, lymphangiogenesis in the intestine wall was totally disrupted in Cdc42 EC knockout embryos. Moreover, we analyzed the role of Cdc42 in lymphatic vessel formation in the skin. We found that Cdc42 is required for tip cells filopodia formation and the deletion of Cdc42 in endothelial cells impaired lymphatic vessel sprouting, branching and the mutant lymphatic vessels displayed blunt-ended, bulbous lymphatic. We also noted that the size of lymphatic lumen was significantly increased. Taken together, our data suggested that Cdc42 plays an essential role in lymphatic branching, maturation and valve formation during development.

D * (Detectivity), an important figure of merit for photodetectors, is limited by zero bias resistance–area product ( R 0 A ) . R 0 A is determined by Auger recombination mechanism, depending on the composition, temperature, carrier concentration and other parameters of the photodetectors. To investigate R 0 A of In1−xGaxAs infrared photodetectors, in this paper, theoretical analysis of Auger recombination mechanism was carried out in the room temperature, by taking CCCH, CHHL and CHHS into account. The calculated results show that there are significant influences on R 0 A for various parameters in both p- and n-type regions of the devices. With carrier concentration around 1017 to 1018 cm−3, R 0 A of 108 Ω cm2 (n-region) and 106 Ω cm2 (p-region) are obtained for x = 0.47 , when thickness and surface recombination velocity of the sample are 5 μm and 100 m/s, respectively.

Fibroblast growth factor 1 (FGF1) has the property to become translocated from the extracellular space into the cell cytosol and nucleus. Membrane translocation of FGF1 occurs subsequent to endocytic uptake and is strictly FGF-receptor (FGFR) dependent. Here we have investigated the timing of FGF1 translocation in relation to FGFR1 signalling. We found that the translocation of FGF1 is a periodic event that occurs with 24h intervals. Serum-starved cells translocated the growth factor with peak occurrences ~6 h, ~30 h, and ~54 h after the addition of FGF1. The periodic FGF1 translocation was totally independent of the FGFR1 tyrosine kinase activity as it proceeded unchanged when the kinase activity was chemically inhibited or the kinase domain was deleted. Furthermore, FGF1 translocation was not restricted to a particular phase of the cell cycle or dependent on cell cycle progression. The results demonstrate that the FGF1/FGFR1 complex constitutes a signalling module that independently of the receptor tyrosine kinase can convey a signal that initiates a strictly timed and periodic release of endocytosed FGF1 into the cytosol/nucleus.

Catalyst-free InP nanowires were grown on Si (1 0 0) substrates by metal-organic chemical vapor deposition. Morphology, crystal structure, photoluminescence, and Raman scattering properties of the nanowires were investigated. Most nanowires are long and straight; the angles between the nanowires and the Si substrate are diverse. The photoluminescence peak shows blue-shift from the band gap energy of bulk InP. Both the blue-shift of photoluminescence peak and the full width at half-maximum of photoluminescence spectrum increase with decreasing nanowires growth temperature. Due to laser-induced heating, the TO and LO phonon peaks of the nanowires reveal downshift and asymmetric broadening compared with those of bulk InP at room temperature.

In 0.82 Ga 0.18 As was grown by LP-MOCVD on InP substrates with the two-step growth technique. It was analyzed that epilayer's growth temperature affected on the crystalline quality, surface morphology, carrier concentration, and mobility of the In 0.82 Ga 0.18 As, which was characterized by X-ray diffraction, scanning electron microscopy, and Hall measurements. The evaluation of stress in In 0.82 Ga 0.18 As was made from frequency shift of the GaAs-like LO phonon of the Raman spectrum.

In 0.8 Ga 0.2 As was grown by low-pressure metalorganic chemical vapor deposition (LP-MOCVD) on InP(1 0 0) substrate with two-step growth technique. Effect of buffer thickness on crystalline quality, surface morphology, electrical property and stress of In 0.8 Ga 0.2 As epilayer was analyzed, and properties of the In 0.8 Ga 0.2 As epilayer were characterized by X-ray diffraction, scanning electron microscopy, Hall measurements and Raman scattering. The experiments showed that the properties of the In 0.8 Ga 0.2 As epilayer had close relation to the buffer thickness and the optimum buffer thickness was about 100 nm.

InAs 0.9 Sb 0.1 epilayers are grown on GaAs (001) substrates by metal organic chemical vapor deposition (MOCVD). In order to relax compressive strain caused by lattice mismatch between InAs 0.9 Sb 0.1 and GaAs, we employ a two-step growth method in which low temperature (430 °C) InAs 0.9 Sb 0.1 buffer layers with different thicknesses are introduced into the structure. Effect of the buffer layer thickness and the epilayer's growth temperature on crystalline quality of the epilayer is investigated, respectively. It is clear that there are strip pyramids paralleling with each other on most surface of the samples. The crystalline quality gets well obviously when the buffer layer thickness change from 0 to 50 nm, but it gets worse when the buffer layer thickness increases to 100 nm. It is also shown that the crystalline quality of the epilayer is improved obviously when the epilayer is grown at 500 °C, and it gets worse when the growth temperature decreases or increases.

An electrophoretic process was developed to selectively assemble carbon nanotubes (CNTs) onto the triode structure and a CNT-based planar-gate-type electron source panel of planar gate stripe was successfully fabricated with the special electrophoretic process. In this process, the CNTs were migrated on cathode electrode in the CNT suspension by an applied voltage between the gate electrode and cathode electrode. The applied voltage was also used to keep the CNTs off adsorbing on the gate electrode. The experiment results show that the CNTs are selectively defined onto cathode electrode and each cathode electrode has the same packing density. In addition, field emission characteristics of the planar-gate-type electron source panel were studied. The anode current densities could be modified from 0 to 216 μA/cm 2 by increasing the gate voltages from 0 to 150 V with anode bias of 1400 V for anode–cathode spacing was 500 μm.

An efficient way to improve field emission characteristic of carbon nanotubes (CNTs) through an Ag micro-particle intermediation layer is presented. In this way, the intermediation layer is deposited on an indium tin oxide glass substrate by electrochemical method and then the CNTs are covered onto surface of the intermediation layer by electrophoretic method as CNT field emitters. The field emission characteristic of the CNT field emitters with the intermediation layer is significantly improved compared to the one without the intermediation layer, including decreased turn-on electric field from 4.2 to 3.1V/@mm and increased emission current density from 0.224 to 0.912mA/cm^2 at an applied electric field of 6V/@mm. The improved field emission characteristic may be attributed to gibbous surface of the CNT field emitters. This efficient way is much simple, low cost, and suitable for production of large scale CNTs-based field emission cold cathode.