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Qiang Sun

Publications and source records attributed to Qiang Sun.

At least 19 recordsLinked to original sources
PubMed2026

Genetic Variation and Evolutionary Characteristics of Coxsackievirus B1: F3 Subtype Associated With Hand, Foot and Mouth Disease in China.

Coxsackievirus B1 (CV-B1) is primarily associated with meningitis but can also cause localized outbreaks of hand, foot, and mouth disease (HFMD). This study analyzed the genetic diversity of the VP1 gene in 39 strains of the CVB1 virus isolated from HFMD children across 15 provinces in China between 2010 and 2024, as well as 179 strains from 17 countries. Based on the average nucleotide difference of VP1 gene, we classified CVB1 virus into six genotypes A to F, Notably, genotype F is newly classified. Since 2010, genotype F guadually replaced genotype E as the dominant genotype in China and has further subdivided into three subtypes: F1, F2, and F3, with F3 being the most prevalent subtype in China currently. We specifically study the mild and severe cases within the F3 subtype. Temperature-sensitivity experiments revealed no differences between mild and severe cases of the F3 subtype, and they all belong to temperature-sensitive strains. Interestingly, we found that mild cases of the F3 subtype did not involve recombination, whereas all severe cases of the F3 subtype showed recombination with Coxsackievirus B4 (CVB4). CVB4 has consistently been the primary pathogen responsible for severe neonatal illnesses, suggesting that recombination between the F3 subtype and CVB4 may be associated with the development of severe HFMD. These findings provide fundamental scientific data for further investigation into the epidemiology and genetic characteristics of variants of Coxsackievirus B1 in China.

Humans↗
PubMed2025

A complete and near-perfect rhesus macaque reference genome: lessons from subtelomeric repeats and sequencing bias.

A truly complete, telomere-to-telomere (T2T), and error-free reference genome remains a foundational resource-and long-standing goal-for unbiased comparative and functional genomics. While recent T2T assemblies of humans and other primates have made substantial progress, most still contain thousands of base-level errors, particularly within highly repetitive regions. Here, we present T2T-MMU8v2.0, a near-perfect T2T assembly of the rhesus macaque (Macaca mulatta), representing the highest base-level accuracy reported in a primate genome to date. By employing an optimized ONT-only assembly strategy, we identify subtelomeric satellite-rich regions as the principal bottleneck to improving assembly quality, owing to technological biases in long-read platforms and limitations in current hybrid assembly frameworks. We discover 268 previously unannotated repeat families and resolve ~8 Mbp of SATR satellite arrays, with over 99-fold enrichment in historically misassembled subtelomeric regions. These satellites form four distinct genomic architectures, each with unique SATR satellite composition, segmental duplication organization, and epigenetic signatures, distinct from the subtelomeric architectures observed in hominid genomes. Notably, in contrast to the largely gene-poor subtelomeric regions in African hominids, the SATR architectures in macaques harbor 58 actively transcribed genes, supported by open chromatin and expression data, suggesting gene innovation within these repetitive regions. Functionally, T2T-MMU8v2.0 improves read mappability and accuracy across sequencing platforms, and results in a 19% improvement of transcription start site enrichment scores and 5,821 additional chromatin accessibility peaks on average, thereby enhancing variant detection, regulatory annotation, and transcriptomic resolution in population genetics or single-nucleus studies. Together, this work establishes a new benchmark for genomics, offers a roadmap for resolving complex repetitive regions, and reveals previously unrecognized features of subtelomeric genome structure and evolution.

Journal Article↗
PubMed2025

Comprehensive discovery and functional characterization of the noncanonical proteome.

The systematic identification and functional characterization of noncanonical translation products, such as novel peptides, will facilitate the understanding of the human genome and provide new insights into cell biology. Here, we constructed a high-coverage peptide sequencing reference library with 11,668,944 open reading frames and employed an ultrafiltration tandem mass spectrometry assay to identify novel peptides. Through these methods, we discovered 8945 previously unannotated peptides from normal gastric tissues, gastric cancer tissues and cell lines, nearly half of which were derived from noncoding RNAs. Moreover, our CRISPR screening revealed that 1161 peptides are involved in tumor cell proliferation. The presence and physiological function of a subset of these peptides, selected based on screening scores, amino acid length, and various indicators, were verified through Flag-knockin and multiple other methods. To further characterize the potential regulatory mechanisms involved, we constructed a framework based on artificial intelligence structure prediction and peptide‒protein interaction network analysis for the top 100 candidates and revealed that these cancer-related peptides have diverse subcellular locations and participate in organelle-specific processes. Further investigation verified the interacting partners of pep1-nc-OLMALINC, pep5-nc-TRHDE-AS1, pep-nc-ZNF436-AS1 and pep2-nc-AC027045.3, and the functions of these peptides in mitochondrial complex assembly, energy metabolism, and cholesterol metabolism, respectively. We showed that pep5-nc-TRHDE-AS1 and pep2-nc-AC027045.3 had substantial impacts on tumor growth in xenograft models. Furthermore, the dysregulation of these four peptides is closely correlated with clinical prognosis. Taken together, our study provides a comprehensive characterization of the noncanonical proteome, and highlights critical roles of these previously unannotated peptides in cancer biology.

Humans↗
PubMed2006

Side-by-side characterization of electron tunneling through monolayers of isomeric molecules: a combined experimental and theoretical study.

We report a new experimental method for measuring relatively small differences in electron tunneling through two distinct monolayers. We place them side by side using scanning probe nanolithography and compare the tunneling currents by conductive probe atomic force microscopy under identical force, voltage, and tip contamination conditions. We demonstrate the validity of our approach by applying it to two isomeric molecules with similar length and functional groups, with only the position of two functional groups, one aromatic and the other aliphatic, being inverted with respect to each other. The relative values of the two tunneling currents, calculated using density functional theory and the Tersoff-Hamann approach, compare very well with the experimental data, providing us with an example of theory vs experiment agreement that is rather uncommon in this field.

Letter↗
PubMed2006

Interface and molecular electronic structure vs tunneling characteristics of CH3- and CF3-terminated thiol monolayers on Au(111).

By means of density functional theory calculations, we investigate work functions, energy level alignments, charge transfers, and tunneling characteristics of CH3- and CF3-terminated alkane- and diphenylthiol monolayers on Au(111). While the alignments of the energy levels and the charge transfers at the metal-molecule interface are found to be determined by the value of the clean Au surface work function relative to the HOMO ionization potential (IP) at the thiolate end of the monolayer, the change of work function for the modified Au(111) surface is dominated by the properties of the thiolate monolayer, including the character, saturated or conjugated, of the molecule and the chemical nature and orientation of the terminal group. The tunneling currents through the adsorbed molecular monolayers are calculated using the Tersoff-Hamann approach. The computed difference between the I-V characteristics for the CH3- and CF3-terminated alkanethiol monolayers agree well with available experimental data. The energy barrier at the metal-molecule interface, the molecular electronic structure, and the IP of the terminal group are the key parameters which determine the tunneling properties.

Journal Article↗
PubMed2006

A single decoy oligodeoxynucleotides targeting multiple oncoproteins produces strong anticancer effects.

Cancer in general is a multifactorial process. Targeting a single factor may not be optimal in therapy, because single agents are limited by incomplete efficacy and dose-limiting adverse effects. Combination pharmacotherapy or "drug cocktail" therapy has value against many diseases, including cancers. We report an innovative decoy oligodeoxynucleotide (dODN) technology that we term complex decoy oligodeoxynucleotide (cdODNs) in which multiple cis elements are engineered into single dODNs attacking multiple target transcription factors, mimicking the drug cocktail approach. We designed dODNs targeting NF-kappaB, E2F, and Stat3 separately and a cdODN targeting NF-kappaB, E2F, and Stat3 concomitantly. We evaluated effects of this cdODN on expression of cancer-related genes, viability of human cancer cell lines, and in vivo tumor growth in nude mice. The cdODN targeting all NF-kappaB, E2F, and Stat3 together demonstrated enhancement of efficacy of more than 2-fold and increases in potency of 2 orders of magnitude compared with each of the dODNs or the combination of all three dODNs. The cdODN also showed earlier onset and longer-lasting action. Most strikingly, the cdODN acquired the ability to attack multiple molecules critical to cancer progression via multiple mechanisms, leading to elimination of regression. Real-time reverse transcription-polymerase chain reaction revealed that the cdODNs knocked down expression of the genes regulated by the target transcription factors. The cdODN strategy offers resourceful combinations of varying cis elements for concomitantly targeting multiple molecules in cancer biological processes and opens the door to "one-drug, multiple-target" therapy for a broad range of human cancers.

Animals↗
PubMed2006

Nuclear accumulation of cRel following C-terminal phosphorylation by TBK1/IKK epsilon.

The NF-kappaB transcription factors are key regulators of immunomodulatory, cell cycle, and developmental gene regulation. NF-kappaB activity is mainly regulated through the phosphorylation of IkappaB by the IkappaB kinase (IKK) complex IKKalphabetagamma, leading to proteasome-mediated degradation of IkappaB, nuclear translocation of NF-kappaB dimers, DNA binding, and gene induction. Additionally, direct posttranslational modifications of NF-kappaB p65 and cRel subunits involving C-terminal phosphorylation has been demonstrated. The noncanonical IKK-related homologs, TNFR-associated factor family member-associated NF-kappaB activator (TANK)-binding kinase (TBK)1 and IKKepsilon, are also thought to play a role in NF-kappaB regulation, but their functions remain unclear. TBK1 and IKKepsilon were recently described as essential regulators of IFN gene activation through direct phosphorylation of the IFN regulatory factor-3 and -7 transcription factors. In the present study, we sought to determine whether IKKepsilon and TBK1 could modulate cRel activity via phosphorylation. TBK1 and IKKepsilon directly phosphorylate the C-terminal domain of cRel in vitro and in vivo and regulate nuclear accumulation of cRel, independently of the classical IkappaB/IKK pathway. IkappaBalpha degradation is not affected, but rather IKKepsilon-mediated phosphorylation of cRel leads to dissociation of the IkappaBalpha-cRel complex. These results illustrate a previously unrecognized aspect of cRel regulation, controlled by direct IKKepsilon/TBK1 phosphorylation.

Amino Acid Sequence↗
PubMed2006

First-principles study of hydrogen storage on Li12C60.

Solid state materials capable of storing hydrogen with high gravimetric (9 wt %) and volumetric density (70 g/L) are critical for the success of a new hydrogen economy. In addition, an ideal storage system should be able to operate under ambient thermodynamic conditions and exhibit fast hydrogen sorption kinetics. No materials are known that meet all these requirements. While recent theoretical efforts showed some promise for transition-metal-coated carbon fullerenes, later studies demonstrated that these metal atoms prefer to cluster on the fullerene surface, thus reducing greatly the weight percentage of stored hydrogen. Using density functional theory we show that Li-coated fullerenes do not suffer from this constraint. In particular, we find that an isolated Li(12)C(60) cluster where Li atoms are capped onto the pentagonal faces of the fullerene not only is very stable but also can store up to 120 hydrogen atoms in molecular form with a binding energy of 0.075 eV/H(2). In addition, the structural integrity of Li(12)C(60) clusters is maintained when they are allowed to interact with each other. The lowest energy structure of the dimer is one where the Li atom capped on the five-member ring of one fullerene binds to the six-member ring of the other. The binding of hydrogen to the linking Li atom and the potential of materials composed of Li(12)C(60) building blocks for hydrogen storage are discussed.

Journal Article↗
PubMed2006

SUMO-1 modification increases human SOD1 stability and aggregation.

The mutations in the gene encoding copper-zinc superoxide dismutase (SOD1) cause approximately 20% cases of familial amyotrophic lateral sclerosis (FALS), characterized by selective loss of motor neurons. Mutant SOD1 forms inclusions in tissues from FALS patients. However, the precise mechanism of the accumulation of mutant SOD1 remains unclear. Here we show that human SOD1 is a substrate modified by SUMO-1. A conversion of lysine 75 to an arginine within a SUMO consensus sequence in SOD1 completely abolishes SOD1 sumoylation. We further show that SUMO-1 modification, on both wild-type and mutant SOD1, increases SOD1 steady state level and aggregation. Moreover, SUMO-1 co-localizes onto the aggregates formed by SOD1. These findings imply that SUMO-1 modification on lysine 75 may participate in regulating SOD1 stability and its aggregation process. Thus, our results suggest that sumoylation of SOD1 may be involved in the pathogenesis of FALS associated with mutant SOD1.

Cell Line↗
PubMed2006

Generation and characterization of a transgenic mouse model for pancreatic cancer.

AIM: To generate a SV40Tag transgenic tumor animal model and to study the mechanism underlying tumorigenesis. METHODS: A mammary gland expression vector containing SV40Tag DNA was generated. Transgene fragments were microinjeted into fertilized eggs of FVB mice. The genetically manipulated embryos were transferred into the oviducts of pseudo-pregnant female mice. PCR and Northern blot analysis were used for genotype analysis of F1 and F2 mice. Transgene expression was detected by RT-PCR and immunohistochemistry. RESULTS: SV40Tag gene was detected in two lines of transgenic mice. One of them delivered the transgene to F1 and a tumor was found in the pancreas of these mice. RT-PCR and immunohistochemistry showed that SV40Tag gene was expressed in the tumor. Pathological characterization of the transgenic mice demonstrated that the tumor belonged to pancreatic cystic neoplasm. CONCLUSION: SV40Tag transgenic mouse model can be successfully established. The transgenic mice develop a pancreatic tumor, which can be used for investigation of the molecular mechanism of tumorigenesis in vivo.

Animals↗
PubMed2006

Association of estrogen receptor gene polymorphisms with susceptibility to adolescent idiopathic scoliosis.

STUDY DESIGN: A case-control study is presented. OBJECTIVE: To investigate the association of estrogen receptor gene polymorphisms with adolescent idiopathic scoliosis (AIS) risk. SUMMARY OF BACKGROUND DATA: Previous studies have shown that genetic factors are important in the pathogenesis of idiopathic scoliosis. Only 1 publication suggested that XbaI site polymorphism was associated with curve severity of idiopathic scoliosis. However, to our knowledge, the relationship of estrogen receptor gene polymorphisms and the individual susceptibility to idiopathic scoliosis has not been studied. METHODS: This study included 202 patients with AIS and 174 healthy controls. Height, menarche status, curve pattern, Cobb angle, and Risser sign in female patients were recorded. There were 2 polymorphic loci, PvuII and XbaI locus, of estrogen receptor analyzed by restriction fragment length polymorphisms. RESULTS: The frequency of XX genotype was significantly higher in patients than that in controls (P = 0.005). The X allele appeared to be overrepresented in patients compared with controls (P = 0.001). Furthermore, the frequencies of XX genotype in female patients whose height was > or = 160 cm and Cobb angle > or = 40 degrees were higher than those whose height was <160 cm and Cobb angle <40 degrees (P = 0.001 and P < 0.001, respectively). CONCLUSIONS: The XbaI site polymorphism of estrogen receptor gene may be associated with a risk of AIS.

Adolescent↗
PubMed2006

[Evaluation of hemodynamic changes by digital subtraction angiography after treatment of avascular osteonecrosis of femoral head with vascularized bone flaps].

OBJECTIVE: To evaluate the effect of digital subtraction angiography (DSA) in evaluation of the hemodynamic changes after treatment of avascular osteonecrosis of femoral head with vascularized bone flaps. METHODS: Fifty-four patients, 33 males and 21 females, 33 hips being at the stage II and 21 hips being at the stage III, were treated with vascularized bone flaps, including iliac bone flaps pedicled with ascending branch of lateral femoral circumflex artery for 23 hips, greater trochanter bone flaps pedicled with gluteal muscle branch of ascending branch of lateral femoral circumflex artery for 13 hips, greater trochanter bone flaps pedicled with transverse branch of ascending branch of lateral femoral circumflex artery for 9 hips, and greater trochanter bone flaps pedicled with gluteal muscle branch and transverse branch of ascending branch of lateral femoral circumflex artery for 9 hips. Selective DSA was performed on all 54 patients pre-operatively and on 19 patients 6-24 months post-operatively. RESULTS: DSA before operation demonstrated abnormal vascularization in all 54 patients. Six months after operation reconstruction of blood supply on the femoral head was seen in 48 cases. Six patients showed poor filling or failure of filling of the vessel pedicles in transplanted bone flaps 6 months post-operatively and DSA conducted 8 months postoperatively showed satisfactory filling in one of the 6 cases. The clinical success rate of this group was 91%, and the radiological success rate was 85%. CONCLUSION: Selective DSA is effective in evaluation of the postoperative hemodynamic changes in the necrotic femoral head. Significant blood supply in the bone flap is the key point in the success of treatment of ONFH.

Adult↗
PubMed2006

Dissociation of a MAVS/IPS-1/VISA/Cardif-IKKepsilon molecular complex from the mitochondrial outer membrane by hepatitis C virus NS3-4A proteolytic cleavage.

Intracellular RNA virus infection is detected by the cytoplasmic RNA helicase RIG-I that plays an essential role in signaling to the host antiviral response. Recently, the adapter molecule that links RIG-I sensing of incoming viral RNA to downstream signaling and gene activation events was characterized by four different groups; MAVS/IPS-1-1/VISA/Cardif contains an amino-terminal CARD domain and a carboxyl-terminal mitochondrial transmembrane sequence that localizes to the mitochondrial membrane. Furthermore, the hepatitis C virus NS3-4A protease complex specifically targets MAVS/IPS-1/VISA/Cardif for cleavage as part of its immune evasion strategy. With a novel search program written in python, we also identified an uncharacterized protein, KIAA1271 (K1271), containing a single CARD-like domain at the N terminus and a Leu-Val-rich C terminus that is identical to that of MAVS/IPS-1/VISA/Cardif. Using a combination of biochemical analysis, subcellular fractionation, and confocal microscopy, we now demonstrate that NS3-4A cleavage of MAVS/IPS-1/VISA/Cardif/K1271 results in its dissociation from the mitochondrial membrane and disrupts signaling to the antiviral immune response. Furthermore, virus-induced IKKepsilon kinase, but not TBK1, colocalized strongly with MAVS at the mitochondrial membrane, and the localization of both molecules was disrupted by NS3-4A expression. Mutation of the critical cysteine 508 to alanine was sufficient to maintain mitochondrial localization of MAVS/IPS-1/VISA/Cardif and IKKepsilon in the presence of NS3-4A. These observations provide an outline of the mechanism by which hepatitis C virus evades the interferon antiviral response.

Adaptor Proteins, Signal Transducing↗
PubMed2006

Tumor necrosis factor alpha enhances influenza A virus-induced expression of antiviral cytokines by activating RIG-I gene expression.

Epithelial cells of the lung are the primary targets for respiratory viruses. Virus-carried single-stranded RNA (ssRNA) can activate Toll-like receptors (TLRs) 7 and 8, whereas dsRNA is bound by TLR3 and a cytoplasmic RNA helicase, retinoic acid-inducible protein I (RIG-I). This recognition leads to the activation of host cell cytokine gene expression. Here we have studied the regulation of influenza A and Sendai virus-induced alpha interferon (IFN-alpha), IFN-beta, interleukin-28 (IL-28), and IL-29 gene expression in human lung A549 epithelial cells. Sendai virus infection readily activated the expression of the IFN-alpha, IFN-beta, IL-28, and IL-29 genes, whereas influenza A virus-induced activation of these genes was mainly dependent on pretreatment of A549 cells with IFN-alpha or tumor necrosis factor alpha (TNF-alpha). IFN-alpha and TNF-alpha induced the expression of the RIG-I, TLR3, MyD88, TRIF, and IRF7 genes, whereas no detectable TLR7 and TLR8 was seen in A549 cells. TNF-alpha also strongly enhanced IKK epsilon mRNA and protein expression. Ectopic expression of a constitutively active form of RIG-I (deltaRIG-I) or IKK epsilon, but not that of TLR3, enhanced the expression of the IFN-beta, IL-28, and IL-29 genes. Furthermore, a dominant-negative form of RIG-I inhibited influenza A virus-induced IFN-beta promoter activity in TNF-alpha-pretreated cells. In conclusion, IFN-alpha and TNF-alpha enhanced the expression of the components of TLR and RIG-I signaling pathways, but RIG-I was identified as the central regulator of influenza A virus-induced expression of antiviral cytokines in human lung epithelial cells.

Cell Line, Tumor↗
PubMed2006

Free iliac crest grafts with periosteum for treatment of old acetabular defects.

OBJECTIVE: To inquire into the therapeutic effectiveness of free iliac crest grafts with periosteum on old acetabular defects. METHODS: From February 1996 to June 2005, 9 patients were treated with free iliac crest grafts with periosteum to reconstruct old acetabular defects. There were 7 males and 2 females and the average age was 41.3 years. The acetabular defects were caused by traffic accidents in 6 cases and fall injury in 3 cases. The time from injury to treatment was 4-13 months and averaged 8 months. Intraoperatively we firstly removed the acetabular fracture fragments of the posterior wall. The femoral head was then reduced. Bone graft was harvested from the iliac crest with periosteum, which was sculpted with a rongeur to conform to the defect. The concave (iliac fossa) side of the graft was placed toward the femoral head. The graft was securely fixed by two to three leg screws. RESULTS: Postoperative syndrome was not found in any of the cases. Harris' score system showed that the score raised from 32.3 points preoperatively to 81 points postoperatively. The hip function was evaluated as excellent in 3 cases, good in 4 cases and fair in 2 cases. CONCLUSIONS: Although this procedure could not exactly reproduce the anatomy of the hip joint, it enables to restore the posterior stability, provide bone-stock for the hip joints and prevent dislocation of the femoral head.

Acetabulum↗
PubMed2005

Defining the mammalian CArGome.

Serum response factor (SRF) binds a 1216-fold degenerate cis element known as the CArG box. CArG boxes are found primarily in muscle- and growth-factor-associated genes although the full spectrum of functional CArG elements in the genome (the CArGome) has yet to be defined. Here we describe a genome-wide screen to further define the functional mammalian CArGome. A computational approach involving comparative genomic analyses of human and mouse orthologous genes uncovered >100 hypothetical SRF-dependent genes, including 10 previously identified SRF targets, harboring a conserved CArG element within 4000 bp of the annotated transcription start site (TSS). We PCR-cloned 89 hypothetical SRF targets and subjected each of them to at least two of several validations including luciferase reporter, gel shift, chromatin immunoprecipitation, and mRNA expression following RNAi knockdown of SRF; 60/89 (67%) of the targets were validated. Interestingly, 26 of the validated SRF target genes encode for cytoskeletal/contractile or adhesion proteins. RNAi knockdown of SRF diminishes expression of several SRF-dependent cytoskeletal genes and elicits an attending perturbation in the cytoarchitecture of both human and rodent cells. These data illustrate the power of integrating existing algorithms to interrogate the genome in a relatively unbiased fashion for cis-regulatory element discovery. In this manner, we have further expanded the mammalian CArGome with the discovery of an array of cyto-contractile genes that coordinate normal cytoskeletal homeostasis. We suggest one function of SRF is that of an ancient master regulator of the actin cytoskeleton.

Animals↗
PubMed2005

Negative regulation of the retinoic acid-inducible gene I-induced antiviral state by the ubiquitin-editing protein A20.

Activation of the interferon regulatory factors (IRFs) 3 and 7 transcription factors is essential for the induction of type I interferon (IFN) and development of the innate antiviral response. Retinoic acid-inducible gene I has been shown to contribute to virus-induced IFN production independent of the Toll-like receptor pathways in response to a variety of RNA viruses and double-stranded RNA. In the present study, we demonstrate that the NF-kappaB-inducible, anti-apoptotic protein A20 efficiently blocks RIG-I-mediated activation of NF-kappaB-, IRF-3-, and IRF-7-dependent promoters but only weakly interferes with TRIF-TLR-3-mediated IFN activation. Expression of A20 completely blocked CARD domain containing DeltaRIG-I-induced IRF-3 Ser-396 phosphorylation, homodimerization, and DNA binding. The level of A20 inhibition was upstream of the TBK1/IKKepsilon kinases that phosphorylate IRF3 and IRF7 and paradoxically, A20 selectively degraded the TRIF protein but not RIG-I. A20 possesses two ubiquitin-editing domains, an N-terminal deubiquitination domain and a C-terminal ubiquitin ligase domain consisting of seven zinc finger domains. Deletion of the N-terminal de-ubiquitination domain had no significant effect on the inhibitory effect of A20, whereas deletion or mutation of zinc finger motif 7 ablated the inhibitory function of A20 on IRF- or NF-kappaB-mediated gene expression. Furthermore, cells stably expressing the active form of RIG-I induced an antiviral state that interfered with replication of vesicular stomatitis virus, an effect that was reversed by stable co-expression of A20. These results suggest that the virus-inducible, NF-kappaB-dependent activation of A20 functions as a negative regulator of RIG-I-mediated induction of the antiviral state.

Adaptor Proteins, Vesicular Transport↗