Analysis of Tumor Necrosis Factor-Alpha (TNF-α) mRNA and Its Receptors in Single Murine Oocytes during Oocyte Meiotic Maturation using Reverse Transcription Polymerase Chain Reaction (RT-PCR)

2012 ◽  
Vol 3 (4) ◽  
pp. 355-362
Author(s):  
Olena A. Shepel ◽  
Viktor E. Dosenko ◽  
Tetyana Yu. Voznesenska ◽  
Roman I. Yanchiy
Keyword(s):  
Tumor Necrosis ◽  
Meiotic Maturation ◽  
Rt Pcr ◽  
Chain Reaction ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Polymerase Chain ◽  
Oocyte Meiotic Maturation ◽  
Necrosis Factor

scholarly journals DETEKSI GEN IL-6 DAN TNF-α DENGAN METODE PCR PADA PENDERITA HEPATITIS B DI LABORATORIUM KLINIK MAXIMA KOTA KENDARI

2021 ◽  
Vol 7 (1) ◽  
pp. 21-28
Author(s):  
Sanatang Abbas ◽  
Sri Anggarini Rasyid ◽  
Tiara Mayang Pratiwi Lio
Keyword(s):  
Tumor Necrosis Factor ◽  
Hepatitis B ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Virus Hepatitis ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Polymerase Chain ◽  
Necrosis Factor

Penyakit Hepatitis B adalah inflamasi yang terjadi pada organ hati yang dapat disebabkan oleh virus hepatitis B. Pada saat terjadi inflamasi sitokin yang ada dalam tubuh akan merespon atau mengenali jenis patogen berupa virus yang masuk ke dalam tubuh. Tumor Necrosis Factor (TNF-α) adalah salah satu sitokin pro-inflamasi yang berperan dalam proses inflamasi hati, dan Interleukin-6 (IL-6) adalah sitokin yang disekresikan dari jaringan tubuh pada fase infeksi akut atau kronik. Tujuan dari penelitian ini adalah untuk mendeteksi gen TNF-α dan IL-6 pada penderita hepatitis B dengan metode polymerase chain reaction (PCR). Jenis penelitian yang digunakan dalam penelitian ini adalah semi kuantitatif, dengan desain penelitian eksperimental. Populasi pada penelitian adalah seluruh penderita suspek yang melakukan pemeriksaan rapid Hepatitis B (HbsAg) di Laboratorium Klinik Maxima Kota Kendari sebanyak 7 orang. Teknik penarikan sampel menggunakan total sampling dengan kriteria inklusi sampel yaitu pasien yang tidak memiliki riwayat penyakit lain selain hepatitis B. Berdasarkan hasil penelitian diketahui bahwa dari ketujuh sampel penderita hepatitis B yang diperiksa menggunakan metode PCR 3 sampel dengan hasil positif (45%) terhadap gen TNF-α dan 7 (100%) hasil negative terhadap gen Interleukin 6 (IL-6). Sehingga dapat di simpulkan bahwa jenis sitokin yang berperan saat terjadi inflamasi ketika seseorang terinfeksi Virus Hepatitis B adalah Tumor Necrosis Factor Alpha (TNF-α).

scholarly journals A polymorphic microsatellite in the tumor necrosis factor alpha promoter identifies an allele unique to the NZW mouse strain.

1990 ◽  
Vol 171 (6) ◽  
pp. 2141-2146 ◽  
Author(s):  
C V Jongeneel ◽  
H Acha-Orbea ◽  
T Blankenstein
Keyword(s):  
Tumor Necrosis ◽  
Genetic Defect ◽  
Inbred Strains ◽  
Mouse Strains ◽  
Chain Reaction ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Polymerase Chain ◽  
Polymorphic Microsatellite ◽  
Necrosis Factor

We have amplified a (CA)n:(GT)n microsatellite from the TNF promoters of a panel of mouse strains using the polymerase chain reaction. The length of the microsatellites was polymorphic, with eight alleles observed among 15 inbred strains bearing seven distinct H-2 haplotypes, and four outbred strains. In B10 congenic strains, the TNF allele detected by microsatellite polymorphism segregated with the MHC, and in recombinant haplotypes (NOD, NZW), it segregated with H-2D. The TNF allele found in the NZW strain (H-2z) was distinct from those of all other haplotypes, consistent with the hypothesis that this strain may carry a genetic defect in TNF production.

scholarly journals Low-Dose UVB Contributes to Host Resistance against Leishmania amazonensis Infection in Mice through Induction of Gamma Interferon and Tumor Necrosis Factor Alpha Cytokines

2002 ◽  
Vol 9 (3) ◽  
pp. 677-686 ◽  
Author(s):  
Noor Mohammad Khaskhely ◽  
Motoyoshi Maruno ◽  
Hiroshi Uezato ◽  
Atsushi Takamiyagi ◽  
Saeef Taher Ramzi ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Low Dose ◽  
Immunohistochemical Analysis ◽  
Rt Pcr ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Ifn Γ ◽  
Necrosis Factor

ABSTRACT UV radiation suppresses the immune response, a fact which raises the question of whether the phenomenon may find practical applications in the outcome of infectious diseases. In this study, BALB/c mice were exposed to low-dose UVB (250 J/m2) from Dermaray M-DMR-100 for 4 consecutive days. Twelve hours after the last UV exposure, groups of mice were injected with 2 × 106 Leishmania amazonensis promastigotes. The development of skin lesions, as assessed by measurement of visible cutaneous lesions, was significantly suppressed in low-dose UVB-irradiated mice compared to nonirradiated controls. In order to characterize the cytokines involved in this phenomenon, BALB/c mice were irradiated with identical doses of UVB, and gamma interferon (IFN-γ), tumor necrosis factor alpha (TNF-α), and interleukin 4 cytokine levels in blood serum and skin were examined at different times by a sandwich enzyme-linked immunosorbent assay, immunohistochemical analysis, and reverse transcription (RT)-PCR. Upregulated expression of serum IFN-γ and TNF-α was observed from 6 to 24 h. Positive results for IFN-γ and TNF-α in UVB-irradiated mice were obtained by immunohistochemical analysis. By RT-PCR, the mRNA expression of both IFN-γ and TNF-α cytokines was detected in a time-dependent manner only in UVB-irradiated mice. Histopathological analysis and electron microscopy revealed that cellular infiltration, tissue parasitism, and parasitophorus vacuoles in irradiated mice were markedly less noticeable than those in nonirradiated controls. These results suggested that low-dose UVB irradiation played a pathogen-suppressing role in Leishmania-susceptible BALB/c mice via systemic and local upregulation of Th1 (IFN-γ and TNF-α) cytokines.

scholarly journals Association of tumor necrosis factor-alpha -308 G/A and -238 G/A polymorphism with diabetic retinopathy: a systematic review and updated meta-analysis.

2020 ◽  
Author(s):  
Wenna Gao ◽  
Ruilin Zhu ◽  
liu yang
Keyword(s):  
Diabetic Retinopathy ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Meta Analysis ◽  
Entire Group ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

Background: Mounting evidence has suggested tumor necrosis factor-alpha (TNF-α) can promote the development of diabetic retinopathy (DR), and TNF-α gene variants may influence DR risk. However, the results are quite different. Objectives: To comprehensively address this issue, we performed the meta-analysis to evaluate the association of TNF-α-308 G/A and -238 G/A polymorphism with DR. Method: Data were retrieved in a systematic manner and analyzed using STATA Statistical Software. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of associations. Allelic and genotypic comparisons between cases and controls were evaluated. Results: For the TNF-α-308 G/A polymorphism, overall analysis suggested a marginal association with DR [the OR(95%CI) of (GA versus GG), (GA + AA) versus GG, and (A versus G) are 1.21(1.04, 1.41), 1.20(1.03, 1.39), and 1.14(1.01, 1.30), respectively]. And the subgroup analysis indicated an enhanced association among the European population. For the TNF-α-238 G/A polymorphism, there was mild correlation in the entire group [the OR(95%CI) of (GA versus GG) is 1.55(1.14,2.11) ], which was strengthened among the Asian population. Conclusion: The meta-analysis suggested that -308 A and -238 A allele in TNF-α gene potentially increased DR risk and showed a discrepancy in different ethnicities.

Tumor Necrosis Factor-α Production-Enhancing Properties of Novel Adamantylalkylthio Derivatives of Some Heterocyclic Compounds

2005 ◽  
Vol 60 (4) ◽  
pp. 471-475 ◽  
Author(s):  
Barbara Orzeszko ◽  
Tomasz Świtaj ◽  
Anna B. Jakubowska-Mućka ◽  
Witold Lasek ◽  
Andrzej Orzeszko ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Heterocyclic Compounds ◽  
Tumor Necrosis ◽  
The Novel ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Factor Α ◽  
Derivatives Of ◽  
Necrosis Factor

Certain adamantylated heterocycles were previously shown to enhance the secretion of tumor necrosis factor alpha (TNF-α) by murine melanoma cells that have been transduced with the gene for human TNF-α and constitutively expressed this cytokine. The stimulatory potency of those compounds depended, among other factors, on the structure of the linker between the adamantyl residue and the heterocyclic core. In the present study, a series of (1-adamantyl)alkylsulfanyl derivatives of heterocyclic compounds was prepared by alkylation of the corresponding thioheterocyles. Of the novel adamantylalkylthio compounds tested in the aforementioned cell line, 2-(2-adamantan-1-ylethylsulfanyl)- 4-methyl-pyrimidine was found to be the most active

scholarly journals Herpes Simplex Virus 1 E3 Ubiquitin Ligase ICP0 Protein Inhibits Tumor Necrosis Factor Alpha-Induced NF-κB Activation by Interacting with p65/RelA and p50/NF-κB1

2013 ◽  
Vol 87 (23) ◽  
pp. 12935-12948 ◽  
Author(s):  
Jie Zhang ◽  
Kezhen Wang ◽  
Shuai Wang ◽  
Chunfu Zheng
Keyword(s):  
Tumor Necrosis Factor ◽  
Ubiquitin Ligase ◽  
Tumor Necrosis ◽  
Nuclear Translocation ◽  
E3 Ubiquitin Ligase ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor ◽  
Hsv 1

NF-κB plays central roles in regulation of diverse biological processes, including innate and adaptive immunity and inflammation. HSV-1 is the archetypal member of the alphaherpesviruses, with a large genome encoding over 80 viral proteins, many of which are involved in virus-host interactions and show immune modulatory capabilities. In this study, we demonstrated that the HSV-1 ICP0 protein, a viral E3 ubiquitin ligase, was shown to significantly suppress tumor necrosis factor alpha (TNF-α)-mediated NF-κB activation. ICP0 was demonstrated to bind to the NF-κB subunits p65 and p50 by coimmunoprecipitation analysis. ICP0 bound to the Rel homology domain (RHD) of p65. Fluorescence microscopy demonstrated that ICP0 abolished nuclear translocation of p65 upon TNF-α stimulation. Also, ICP0 degraded p50 via its E3 ubiquitin ligase activity. The RING finger (RF) domain mutant ICP0 (ICP0-RF) lost its ability to inhibit TNF-α-mediated NF-κB activation and p65 nuclear translocation and degrade p50. Notably, the RF domain of ICP0 was sufficient to interact with p50 and abolish NF-κB reporter gene activity. Here, it is for the first time shown that HSV-1 ICP0 interacts with p65 and p50, degrades p50 through the ubiquitin-proteasome pathway, and prevents NF-κB-dependent gene expression, which may contribute to immune evasion and pathogenesis of HSV-1.

scholarly journals Analysis of Subcellular RNA Fractions Revealed a Transcription-Independent Effect of Tumor Necrosis Factor Alpha on Splicing, Mediated by Spt5

2016 ◽  
Vol 36 (9) ◽  
pp. 1342-1353 ◽  
Author(s):  
Gil Diamant ◽  
Tal Eisenbaum ◽  
Dena Leshkowitz ◽  
Rivka Dikstein
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Independent Effect ◽  
Necrosis Factor Alpha ◽  
Pol Ii ◽  
Tnf Α ◽  
Factor Alpha ◽  
Induced Genes ◽  
Necrosis Factor

The proinflammatory cytokine tumor necrosis factor alpha (TNF-α) modulates the expression of many genes, primarily through activation of NF-κB. Here, we examined the global effects of the elongation factor Spt5 on nascent and mature mRNAs of TNF-α-induced cells using chromatin and cytosolic subcellular fractions. We identified several classes of TNF-α-induced genes controlled at the level of transcription, splicing, and chromatin retention. Spt5 was found to facilitate splicing and chromatin release in genes displaying high induction rates. Further analysis revealed striking effects of TNF-α on the splicing of 25% of expressed genes; the vast majority were not transcriptionally induced. Splicing enhancement of noninduced genes by TNF-α was transient and independent of NF-κB. Investigating the underlying basis, we found that Spt5 is required for the splicing facilitation of the noninduced genes. In line with this, Spt5 interacts with Sm core protein splicing factors. Furthermore, following TNF-α treatment, levels of RNA polymerase II (Pol II) but not Spt5 are reduced from the splicing-induced genes, suggesting that these genes become enriched with a Pol II-Spt5 form. Our findings revealed the Pol II-Spt5 complex as a highly competent coordinator of cotranscriptional splicing.

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