This level, http://www.selleckchem.com/products/crenolanib-cp-868596.html though high, is within the range attained by human alcoholics. All cultures were terminated 46 hrs from the begin ning of treatment. The concentration of ethanol in the medium was assayed at three time points on each day in a separate group of embryos not used for the analyses, to avoid the potential confounding effects of drawing samples from the cultures. Media samples from alcohol or vehicle treated cultures were assayed in duplicate for alcohol concentrations using an Analox alcohol analyzer. At the end of culture, viability was confirmed by observing the blood circulation of the yolk sac and the beating heart. Cultured embryos were quickly immersed in 0. 7 ml TRIzol and homo genized for extracting total RNA for the RT PCR and microarray processes, or fixed in 4% paraformaldehyde in PBS for the evaluation of the developmental status.

Whole embryos were used because the dysmorphology is observed throughout tissue derived from the three germ layers and in various developing organs. Also, dissection of the millimeter size embryos would unavoidably introduce another source of variabil ity, whole embryos yield sufficient total RNA for single embryo analysis, whereas dissected tissues yield too little RNA and would require pooling or amplification for microarray analysis. Although this limits the resolution of genes contributing to different topographic changes, we thought that obtaining a complete gene expression profile in parallel with this widespread alcohol induced teratogenesis in the embryo would be informative.

Embryonic dysmorphology The analysis of embryo dysmorphology was performed as described by van Maele Fabry et al. and in our previous report. The morphological features of the developing embryo, including the allantois, flexion, heart, caudal neural tube, hind brain, midbrain, fore brain, otic system, optic system, branchial bars, maxil lary process, mandibular process, forelimb, hindlimb, and somites, were examined and scored for any malfor mations using the ordinal scales of our previous report. Scores for each of the above features were typically not normally distributed, so they were analyzed statisti cally by the non parametric Mann Whitney U test. The number of somites was normally distributed, so those data were analyzed by Students t test, using StatView software. Gene expression analyses Two microarray experiments were performed.

In Experi ment 1, total RNA was isolated from individual whole embryos. Each embryo was immediately immersed in 700 ml TRIzol and homogenized using a Polytron. Extrac tion followed the AV-951 TRIzol protocol. Ethanol precipitated RNA was resuspended in DEPC water. RNA was cleaned up using RNeasy mini kit The quality of RNA was assessed by the Agilent Bioanalyzer and by spectrophotometry from 220 nm to 350 nm, concentration was determined from A260.

Those sequences that did not produce a significant hit with the nr database were compared to the PFAM database for annotation. The latter comprises a large collection of multiple sequence alignments and hidden Markov mod els covering many common protein domains. Signif icant BLAST results against TAIR database were used for functional gene ontology annotation. Transcriptome comparison, selleck chemical A. tuberculatus vs. A. hypochondriacus The raw sequence files derived from the recently reported A. tuberculatus transcriptome pyrosequencing effort were downloaded directly from the NCBI Sequence Read Archive at Traces sra sra. cgi study SRP002251. Reads were assembled after quality control, following an identical Tran script annotation for A. tuberculatus was performed by querying the UniRef 100, and Amaranthaceae ESTs databases.

Both transcriptomes were then aligned with each other using BLASTN to identify homologous con tigs. Sequence homology was defined only at E values 1 �� 10 10 and identity 90%. Homologous transcripts were quantified and classified into five different cate gories, i. e. those, i producing the same hit, ii different hits, iii and iv one hit for one species and no hit for the other, and vice versa, or v no hit, when queried against the above databases. Annotated transcripts detected only in A. hypochondriacus or A. tuberculatus were also quantified. Digital expression analysis The number of reads per gene was counted in each of the 454 sequencing outputs derived from the salt stress, water stress, insect herbivory and bacterial infection treatments and also from stem tissue.

Genes having read counts lower than 5 were eliminated. To calculate relative expression profiles in each stress treatment, Rela tive Abundance values were computed for each gene per treatment sample by dividing its 454 sequence count by the total 454 sequence count in the treatment sample. Differentially expressed genes in one or more treatments were detected by using the R and c2 test statistics using a freely available web tool. A gene was considered to be differentially expressed when at least one statistical test yielded significance values 0. 0001. A similar procedure was employed to identify transcripts that were stem speci fic or highly abundant in this tissue.

The following considerations were adopted for the organization of the digital stress related gene expression data, i a minimum or baseline control expression value for a given Anacetrapib gene was assigned to the lowest RA in the four treatment set examined. The RAs that produced an expression ratio 2 when divided by MIN were also considered as MINs, ii a gene was considered to be sig nificantly expressed by a given treatment when its RA yielded a ratio 2 when divided by MIN, and iii maximum expression levels for a given gene were assigned to the treatment having the highest SE. Treat ments were reported to produce additional MEs when their respective SEs yielded a ratio 2 when divided by ME.

tuberculosis infected bone marrow derived macrophages as well as Salmonella infected RAW264. 7 macrophages. Here we report for the first time that B. pseudomallei up regulates both arginase 1 and arginase 2 isoforms in the host with arginase 2 being more dominant. The expression profiles demonstrate both full article host nitric oxide synthase 2 and arginase 2 were elevated at a similar magnitude at 24 hpi. This suggests that arginase competes with NOS2 to produce NO from arginine during the infection, leading to the suboptimal antibacterial effect of NOS2 in the B. pseu domallei infected host. Certain pathogens evade the host defence by trigger ing the TLR2 mediated biased anti inflammatory effects or prevent recognition by TLRs. For example, Yer sinia and Candida induced TLR2 signalling leads to the release of IL 10, which can lead to immunosuppression.

However, the response following recognition of B. pseu domallei via the TLR2 signalling pathway is contrary to the evasion mechanism exploited by Yersina spp. and Candida spp. In addition, some pathogens have devel oped strategies to either block or avoid their recognition by TLRs and subsequent activation of the innate defence. This study suggests that B. pseudomallei may use specific TLR mediated signals to escape from the host defence. Future studies will be aimed at determin ing whether B. pseudomallei utilizes these signals to evade TLR clearance mechanisms. Tissue injury leads to extracellular matrix breakdown, including the degradation of hyaluronic acid and resulting oligosaccharides.

In this study, the gene encod ing hyaluronan synthase 2, the enzyme that pro duces HA, was induced. In contrast, the genes encoding hyaluronoglucosaminidases, the enzymes that degrade HA, were repressed, indicating that perhaps HA is not degraded during a B. pseudomal lei infection. These endogenous signals can also trigger TLR2 and or TLR4 activation and signals distinct from microbial stimulators, for instance HA but not LPS, sig nal through TLR4, MD2, and CD44. Up regulation of TLR2, TLR4 and TLR7 as well as MD2 could indicate B. pseudomallei infected host responses to endogenous signals released during tissue damage. However, the ability of the engaged TLRs to distinguish between microbial and endogenous signals and subsequently trig ger appropriate responses, remains unclear.

These observations reflect that the inflammatory response may cause more damage to the host than the microbe. In summary, our work has provided an exten sive description of host defence responses to B. pseudo mallei during an acute infection. Changes in host cell metabolism as a consequence of nutrient scavenging by intracellular B. pseudomallei have never been studied. Batimastat The microarray data presented here provides the first description of changes in the B.

Among these, genes involved in lipid metabolism and, particularly, in LC PUFA biosynthesis, were found to be together up regulated in fish fed VD. Not surprisingly, delta 6 desaturase, steroyl CoA desaturase 9 and NADH cytochrome b5 reductase, involved in long chain fatty acid desaturation and or elongation, were up regulated in VD fed fish. It is indeed established that in most fish species that the LC PUFA biosynthetic pathway is posi tively regulated in response to the use of a diet poor in LC PUFA but rich in PUFA, although this regulation depends on fish species, degree of fish oil substitution, nature of the vegetable oil, and environmental para meters. The positive regulation of the LC PUFA biosynthetic pathway is in agreement with results obtained by tran scriptomic approaches in salmonids fed vegetable oil.

Altogether, the expression data obtained in mar ine fish species and salmonids indicate that the different capacity of marine and fresh water species to grow on a LC PUFA deprived diet does not seem to be due to a dif ferent transcriptional regulation of key genes involved in lipid synthesis, such as fads2 or scd9. Indeed, the level of induction of fads2 expression found in this experiment is of similar amplitude to that observed in the liver and intestine of Atlantic salmon. The stimulation of this biosynthetic pathway in fish fed a diet poor in LC PUFAs can be explained by the fact that LC PUFAs play several key physiological roles in vertebrates, particularly in fish.

For example, fish are poikilothermic organisms and therefore need a high degree of unsaturation of LC PUFA included in mem brane phospholipids to maintain phospholipid bilayer fluidity at reduced temperature. LC PUFA, espe cially arachidonic acid and eicosapentaenoic acid, are also precursors of eicosanoids, which are involved in pro and anti inflammatory pathways. This hypothesis is reinforced by our data, indicating a stimulation of genes involved in phospholipids bio synthesis when fish were fed the VD. Despite this stimulation of LC PUFA and the phos pholipid biosynthesis pathway at the transcriptional level, our investigation of fatty acid profiles indicated that the amounts of LC PUFA, particularly eicosapen taenoic acid and docosahexaenoic acid, were still considerably lower in the flesh of fish from both half sibfamilies fed VD in comparison with fish fed FD.

This finding is in agreement with those previously obtained, which revealed that the stimulation of fads2 expression in fish fed a vegetable diet was not associated with an induction of its enzymatic activity, suggesting a post transcriptional regulation of fads2 expression. Such EPA and DHA deficiency can notably explain the growth deficiency observed in fish fed VD, as well as effects Drug_discovery observed on immune function.

After additional one hour of incubation, cells were har vested and early viral DNA was measured by real time PCR as described by Popik et al. Statistical analysis Statistical analysis was assessed by Students t test. A value of p 0. 05 was considered significant. Background Lipids over accumulation selleck chemical in the heart are associated with cardiac dysfunction and heart failure. Satu rated fatty acid such as palmitate but not mono unsaturated oleate induced apoptosis in many cell types including the cardiomyocytes element of the heart. Several studies showed that high levels of palmitate had caused significant increases of ceramide and mitochondrial cytochrome c release levels, which was accompanied by significant caspase 3 activation and apoptosis, and this lipotoxicity effect on cardiac myocytes apoptosis remains incompletely understood.

Cardiomyocytes apoptosis is an important contributor to myocardial dysfunction and heart failure, and blockade of myocardial apoptosis results in significant prevention of diabetes induced cardiac dysfunction. Adiponectin is an adipokine secreted from adipose tissue and plasma with concentrations ranging from 3 to 30 ug/mL in mouse and human. The structure of adiponectin contains a collagen repeat domain at the N terminus and a globular domain at the C terminus with a sequence homology to compliment factor C1q. The C terminal globular C1q domain of adiponectin is proteolytically cleaved from the full length protein and is also able to circulate in both human and mouse plasma to mediate potent physiological effects.

Recently, a number of studies have shown that adiponectin tran scripts are synthesized by cardiomyocytes, which are upregulated in mouse models of myocardial injury. To date, adiponectin has been extensively documented to mediate several cardioprotective properties, and anti apoptotic effect of adiponectin on the heart. Phosphatidylinositol 3 kinase /Akt and extracellu lar signaling regulated kinase /mitogen activated protein kinase signaling pathways are an import ant for intracellular signal transduction system. PI3K/Akt has been shown to play a major role in the prevention of apoptosis, and ERK1/2 is a well known taking part in a signal transduction cascade in response to extracellular stimuli, and plays an important role in cell proliferation, growth and cell death.

Several studies have exhibited that anti apoptotic effect of adiponectin on the heart, which appeared to be mediated via PI3K/Akt, ERK1/ 2MAPK and AMP activated protein kinase sig naling pathway. Adiponectin could protect against acute cardiac injury by attenuating the apoptosis, but the mechanism involved the effect of adiponectin in palmitate induced apoptosis are not fully understood. In the present study, we demonstrated AV-951 that adiponectin protected H9c2 cells from palmitate induced apoptosis through both PI3K/Akt and ERK1/2 signaling pathways.

The function of wtp53 is depressed by http://www.selleckchem.com/products/baricitinib-ly3009104.html mp53 in a way that mp53 forms heterogeneous tetramer with wtp53. This ef fect of mp53 is the dominant negative effect. From this, one possibility is that glycerol may depress the dom inant negative effect of mp53 and p53 centered signal transduction may be restored by glycerol. However, we have already reported that WAF1 expression after heating was induced in Saos 2 cells transfected with mp53 gene, when the cells were pre treated with glyc erol. WAF1 expression was not induced even after com bined treatment with heat and glycerol in the cells transfected with neo vector alone without mp53 gene. At least, mp53 is necessary for induction of WAF1 gene ex pression by heat in glycerol treated cells. These results strongly support that the conformation of mp53 was re stored to normal type of p53 by glycerol.

Furthermore, to confirm the conformational change of mp53 to wtp53 suggested by Western blot analysis, the DNA binding activity of p53 for p53CON was measured in nuclear proteins extracted from A 172/neo or A 172/ mp53/248 cells using the gel mobility shift assay. It is known that wtp53 can bind to p53CON homologous to a specific DNA sequence located upstream of the bax gene which positively controls apoptosis. In agreement of this, the binding activity of wtp53 significantly increased in A 172/neo cells treated with heat or combination of heat and glycerol. In contrast, a slight increase in the DNA binding activity of the nuclear proteins was ob served when A 172/mp53/248 cells were treated with heat.

The in crease may be due to endogenous wtp53 in A 172/mp53/ 248 cells. The defective DNA binding ability of p53 from heat treated A 172/mp53/248 cells may be due to the dominant negative nature of mp53 protein. It is known that mp53 has no ability to induce apoptosis, be cause most mp53 can not bind to a specific DNA sequence. On the other hand, when A 172/mp53/248 cells were heated in the presence of glycerol before heating, they showed clear increased DNA binding activi ty of p53 to p53CON. This result shows that mp53 underwent conformational change to wtp53. The enhanced heat sensitivity observed in glycerol pretreated A 172/mp53/143 cells might be induced through bax gene expression up regulat ed by the activated mp53.

No binding activity of p53 was observed when whole cell proteins extracted from intact A 172/neo or A 172/mp53/248 cells were treated with heat, heat plus glycerol or heat plus glycerol plus wort mannin. Thus, the acquisition of binding activity of wtp53 or glycerol treated Dacomitinib mp53 is likely to demand cellular signal transduc tion as described above. Furthermore, the increased DNA binding activity of nuclear proteins from A 172/neo or A 172/mp53/248 cell was suppressed by wortmannin.

In contrast, in MEFDKO barr2, PAR2 stimulated AMPK phosphory lation was inhibited. Furthermore, when flag b arrestin 2 was over expressed in NIH3T3 cells, PAR2 stimulated AMPK phosphorylation was abolished. In NIH3T3 cells over expressing b arrestin 2, we observe a small selleck chemical Trichostatin A increase in base line pAMPK. We do not yet know the significance of this alteration in basal AMPK phosphorylation but may reflect a PAR 2 independent effect of b arrestin on AMPK phosphorylation. b arrestins are involved in ter minating the signals of a number of receptors known to activate AMPK. PAR2 is relatively unusual in that it pro motes a number of b arrestin dependent signaling events, while its G protein signal is being dampened. We conclude that b arrestins can inhibit PAR2 stimu lated AMPK phosphorylation.

PAR2 promotes b arrestin dependent inhibition of AMPK in primary fat To confirm the inhibitory role of b arrestin 2 on AMPK phosphorylation in primary cells, we investigated PAR2 stimulated AMPK phosphorylation in adipose tissue from wild type and either b arrestin 1 or b arrestin 2 mice. AMPK activity in adipose plays a key role in modulating the metabolic state of the animal and we observe high levels of b arrestin expression in primary fat as well as differentiated 3T3L1 adipocytes. Isolated epididymal fat was incubated with or without 2fAP for 5 and 120 minutes, then homogenized and analyzed by SDS PAGE followed by western blotting for phospho AMPK. In wt and b arr1 fat, no significant increase in AMPK activity was observed in response to PAR2 activa tion.

However, in b arr2 fat, PAR2 promoted a 5 fold increase in AMPK phosphorylation, and a 1. 5 2. 5 fold increase in AMPK activity. Similar results were observed in liver from wt, b arr 1 and b arr2 animals. Pretreatment with STO 609 abolished PAR2 stimulated AMPK phosphory lation in b arr2 fat, suggesting that AMPK phosphorylation by CAMKKb is inhibited by b arrestin 2. Consistent with these observations, PAR2 stimulated phosphorylation of the AMPK substrate, ACC, was only observed in b arr2 mice. We conclude that PAR2 can promote CAMKKb depen dent AMPK activation in primary fat, but under normal conditions this activity is suppressed by an inhibitory PAR2 pathway through b arrestin 2. AMPK and CAMKKb associate with b arrestin 2 Our studies on PI3K suggest that b arrestins can form inhibitory scaffolds leading to decreased kinase activity.

To examine whether b arrestins similarly associate with AMPK and CAMKKb, we performed co immunopreci pitations in NIH3T3 cells transfected with flag tagged b arrestin 1 or b arrestin 2, treated with and without 2fAP. Both AMPK and CAMKKb could be co precipi tated with b arrestin 2 and to a lesser extent, b arrestin 1. Only b arrestin 2 increased association GSK-3 with AMPK and CAMKKb upon PAR2 activation. Furthermore, a greater amount of both proteins asso ciated with b arrestin 2 relative to its expression level, than with b arrestin 1.

These are the downregulation of pro neural bHLH factor Ascl1 and the upregulation of Shh and Gli1 mRNAs. Ascl1 downregulation www.selleckchem.com/products/17-DMAG,Hydrochloride-Salt.html could result indirectly through the mod ulation of upstream activators such as Tlx. ChIP data suggests direct HDACi effects at the Shh loci account for the increase in transcription of Shh and its target Gli1. The fact that Shh Gli1 upregulation is accompanied by G1 arrest in our study suggests the mitogenic effects of Shh in adult NSCs require normal HDAC function. In addition to activating cell lineage commitment pro grams, HDACi also promote the re setting of multipotency in terminally differentiated cell lineages by increasing induced pluripotent stem cell re pro gramming efficiency. Somatic cell re program ming reactivates expression of Nanog, a homeobox transcription factor necessary for maintaining multipo tency in embryonic stem cells.

In ES cells, mSin3A HDAC complex at the Nanog promoter acts to positively regulate Nanog expression under proliferating conditions and HDAC inhibition by TSA downregulates Nanog expression, a finding that is analogous to SAHA and NaB repression of multipotent factors in our adult mouse NSC cultures. In our study both SAHA and NaB downregulate the expression of the stem cell maintaining factor Sox2 in adult mouse NSCs. Conditional gene deletion in mice reveals Sox2 is negatively regulated by Hdac2 in adult neuroblasts and that Sox2 repression is necessary for adult neurogenesis Hdac2 neuroblasts ectopically maintain Sox2 expression, fail to mature into neurons and ultimately die of apoptosis.

Taking our data into consideration, HDAC regulation of Sox2 expression in adult NSC lineage progression appears to be biphasic in the first phase, class I and or class II HDAC activity is required to maintain Sox2 expression and the mainte nance of stem progenitor programs in self renewing NSCs. in the second phase, HDAC2 functions to down regulate Sox2 in neuroblasts and permit the full activa tion of neuronal differentiation programs. SAHA treatment leads to cell fate changes in differentiated adult NSCs Our cell fate analysis revealed SAHA treatment of adult NSCs under proliferation culture conditions lead to the long term suppression of glial and oligodendro cyte cell fate markers GFAP and Olig2 in cells induced to differentiate. Using Olig1 Cre and floxed Hdac1 and Hdac2 mice, Ye et al. showed combined dele tion of Hdac1 and Hdac2 in oligodendrocyte progeni tor cells inhibited oligodendrocyte differentiation by repressing Olig2 expression. This effect was mediated by the stabilization Dacomitinib and nuclear translocation of b catenin, which in turn nega tively regulates oligodendrocyte development by repressing Olig2 expression.

miRNA Indirect Functional Analysis Since miRNAs are not included in any ontology data base, we performed an indirect functional analysis by screening the functional terms associated with the experimentally validated selleck chemicals target coding genes of the miR NAs, extracted from TarBase. Once the target nno tated via GO terms or SP keywords, as above. mRNa miRNA Complex Functional Annotation We then checked the functional classifications coher ence between the indirect and direct functional analysis, within each significantly annotated factor. Thus, globally speak ing, F1 annotation is unchanged and related to functions that are responsible for signal transduction. In F2?, 3 out of 7 target coding genes are annotated with terms that can be asso ciated to the categories significantly varied in the mRNA functional analysis, F2? is then confirmed to be a factor involved in functions related with adhesion and or che motaxis.

For the miRNAs in F3, 5 out of 8 target cod ing genes are functionally related with the gene expression term found in the mRNA functional analysis. Interestingly, most of the terms are related with mechanisms of transcription regulation and only one with protein ubi quitination. After direct and indirect annotation, 2 miR NAs and 31 human coding genes in F3 were selected as belonging to the same category. Not surprisingly, most of the coding genes in this list are not predicted to be targets of the 2 miRNAs that appear in the factor. In fact, the biological meaning of the result is a set of genetic elements that share cov ariability in the expression pattern and we know that, e.

g. in animals, most of the control on gene expression is performed by tuning translation. Therefore, the levels of miRNAs and the mRNAs of direct targets are not directly correlated. As it is also suggested in we can imagine that our list of coding genes contains the possible subset of indirect targets of two miRNAs, miR 17 5p, and miR 20b. Globally, F3 is confirmed to be associated with gene expression, with transcription regulation being the most common mechanism of expression. Emergent Properties Since the transcription regulation term appears to give the clearest biological information, coherent in mRNAs and miRNA, we focused our efforts on this part of the analysis. The total sets of mRNAs and miRNAs returned from this analysis are listed in Table S6 and S7 of the Additional file 1.

Latent Structure Chromosomal Loca lization, Most of the miRNAs in F3 belong to two poly cistronic miRNA genes where miRNAs are lying in close proximity on the chromosome. These polycistronic Drug_discovery miRNA genes are involved in cell proliferation, apoptosis suppression, tumor angiogenesis and T cell leukemia. The first polycistronic gene is composed by 7 miRNAs and maps on Chromosome 13 whereas the second one maps on Chromosome �� and contains 6 miRNAs, details are shown in Figure 1.

The effect of HPV 16 E2 on gC1qR e pression, the p38 MAPK JNK signalling pathway and apoptosis in gC1qR silenced cervical squamous carcinoma cells To further e plore the effect of HPV 16 E2 on gC1qR e pression, the p38 MAPK JNK signalling pathway and apoptosis in gC1qR silenced cervical squamous carcin oma cells, C33a and SiHa Rapamycin WY-090217 cells were treated with unmodified media or HPV 16 E2 vector. After 72 h, the cells were transfected with 100 ng of gC1qR siRNA or 100 ng of negative siRNA. gC1qR gene and protein e pression levels were analysed by real time PCR and Western blot analysis. The results demonstrated that gC1qR mRNA and protein e pression levels were signifi cantly increased in the HPV 16 E2 vector group com pared with the unmodified media group.

However, there was no difference between the HPV 16 E2 gC1qR siRNA group and the unmodified media group. gC1qR e pression in the HPV 16 E2 gC1qR siRNA treated group was significantly lower than that in the HPV 16 E2 group. In contrast, gC1qR e pression was notably increased in the HPV 16 E2 negative siRNA group compared with the HPV 16 E2 gC1qR siRNA group. Phospho p38 MAPK and phospho JNK were assessed by Western blot analysis in cervical squamous carcin oma cells that were treated with unmodified media or HPV 16 E2 vector. After 72 h, the cells were transfected with 100 ng of gC1qR siRNA or 100 ng of negative siRNA. As shown in Figure 3C, phospho p38 MAPK and phospho JNK were significantly increased in the HPV 16 E2 group and the HPV 16 E2 negative siRNA group compared with the unmodified media group.

There was no difference in p p38 MAPK and p JNK protein e pression between the unmodified media group and the HPV 16 E2 gC1qR siRNA group. However, the phosphorylated p38 MAPK and JNK protein were notably lower in the HPV 16 E2 gC1qR siRNA group compared with the HPV 16 E2 negative siRNA group. C33a and SiHa cell apoptosis was assessed by flow cy tometry following treatment with unmodified media or HPV 16 E2 vector. After 72 h, GSK-3 the cells were transfected with 100 ng of gC1qR siRNA or 100 ng of negative siRNA. The cells were double stained with Anne in V and PI. Early and late apoptotic cells were distributed in the Q1 LR and Q1 UR regions, respect ively. Necrotic cells were located in the Q1 UL region.

Figure 3D shows that accumulated HPV 16 E2 increased the C33a and SiHa cell number in the Q1 LR and Q1 UR regions in the HPV 16 E2 vector group and the HPV 16 E2 negative siRNA group compared with the unmodified media group. However, the Q1 LR and Q1 UR regions in the HPV 16 E2 gC1qR siRNA vector transfected cells showed a notable decrease com pared with the HPV 16 E2 vector Cabozantinib transfected group. However, the apoptotic cells in the HPV 16 E2 gC1qR siRNA group were significantly decreased compared with the HPV 16 E2 negative siRNA group.