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Category Archives: Gene Medicine

BENITEC BIOPHARMA INC. Management’s Discussion and Analysis of Financial Condition and Results of Operations (form 10-Q) – Marketscreener.com

Posted: February 13, 2023 at 8:00 pm

BENITEC BIOPHARMA INC. Management's Discussion and Analysis of Financial Condition and Results of Operations (form 10-Q)  Marketscreener.com

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CENTOGENE to Participate in Upcoming Conferences in February in the Lead Up to Rare Disease Day – Marketscreener.com

Posted: February 7, 2023 at 6:53 am

CENTOGENE to Participate in Upcoming Conferences in February in the Lead Up to Rare Disease Day  Marketscreener.com

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Gene | Definition, Structure, Expression, & Facts | Britannica

Posted: January 27, 2023 at 8:18 pm

Summary

gene, unit of hereditary information that occupies a fixed position (locus) on a chromosome. Genes achieve their effects by directing the synthesis of proteins.

In eukaryotes (such as animals, plants, and fungi), genes are contained within the cell nucleus. The mitochondria (in animals) and the chloroplasts (in plants) also contain small subsets of genes distinct from the genes found in the nucleus. In prokaryotes (organisms lacking a distinct nucleus, such as bacteria), genes are contained in a single chromosome that is free-floating in the cell cytoplasm. Many bacteria also contain plasmidsextrachromosomal genetic elements with a small number of genes.

The number of genes in an organisms genome (the entire set of chromosomes) varies significantly between species. For example, whereas the human genome contains an estimated 20,000 to 25,000 genes, the genome of the bacterium Escherichia coli O157:H7 houses precisely 5,416 genes. Arabidopsis thalianathe first plant for which a complete genomic sequence was recoveredhas roughly 25,500 genes; its genome is one of the smallest known to plants. Among extant independently replicating organisms, the bacterium Mycoplasma genitalium has the fewest number of genes, just 517.

A brief treatment of genes follows. For full treatment, see heredity.

Genes are composed of deoxyribonucleic acid (DNA), except in some viruses, which have genes consisting of a closely related compound called ribonucleic acid (RNA). A DNA molecule is composed of two chains of nucleotides that wind about each other to resemble a twisted ladder. The sides of the ladder are made up of sugars and phosphates, and the rungs are formed by bonded pairs of nitrogenous bases. These bases are adenine (A), guanine (G), cytosine (C), and thymine (T). An A on one chain bonds to a T on the other (thus forming an AT ladder rung); similarly, a C on one chain bonds to a G on the other. If the bonds between the bases are broken, the two chains unwind, and free nucleotides within the cell attach themselves to the exposed bases of the now-separated chains. The free nucleotides line up along each chain according to the base-pairing ruleA bonds to T, C bonds to G. This process results in the creation of two identical DNA molecules from one original and is the method by which hereditary information is passed from one generation of cells to the next.

The sequence of bases along a strand of DNA determines the genetic code. When the product of a particular gene is needed, the portion of the DNA molecule that contains that gene will split. Through the process of transcription, a strand of RNA with bases complementary to those of the gene is created from the free nucleotides in the cell. (RNA has the base uracil [U] instead of thymine, so A and U form base pairs during RNA synthesis.) This single chain of RNA, called messenger RNA (mRNA), then passes to the organelles called ribosomes, where the process of translation, or protein synthesis, takes place. During translation, a second type of RNA, transfer RNA (tRNA), matches up the nucleotides on mRNA with specific amino acids. Each set of three nucleotides codes for one amino acid. The series of amino acids built according to the sequence of nucleotides forms a polypeptide chain; all proteins are made from one or more linked polypeptide chains.

Experiments conducted in the 1940s indicated one gene being responsible for the assembly of one enzyme, or one polypeptide chain. This is known as the one geneone enzyme hypothesis. However, since this discovery, it has been realized that not all genes encode an enzyme and that some enzymes are made up of several short polypeptides encoded by two or more genes.

Experiments have shown that many of the genes within the cells of organisms are inactive much or even all of the time. Thus, at any time, in both eukaryotes and prokaryotes, it seems that a gene can be switched on or off. The regulation of genes between eukaryotes and prokaryotes differs in important ways.

The process by which genes are activated and deactivated in bacteria is well characterized. Bacteria have three types of genes: structural, operator, and regulator. Structural genes code for the synthesis of specific polypeptides. Operator genes contain the code necessary to begin the process of transcribing the DNA message of one or more structural genes into mRNA. Thus, structural genes are linked to an operator gene in a functional unit called an operon. Ultimately, the activity of the operon is controlled by a regulator gene, which produces a small protein molecule called a repressor. The repressor binds to the operator gene and prevents it from initiating the synthesis of the protein called for by the operon. The presence or absence of certain repressor molecules determines whether the operon is off or on. As mentioned, this model applies to bacteria.

The genes of eukaryotes, which do not have operons, are regulated independently. The series of events associated with gene expression in higher organisms involves multiple levels of regulation and is often influenced by the presence or absence of molecules called transcription factors. These factors influence the fundamental level of gene control, which is the rate of transcription, and may function as activators or enhancers. Specific transcription factors regulate the production of RNA from genes at certain times and in certain types of cells. Transcription factors often bind to the promoter, or regulatory region, found in the genes of higher organisms. Following transcription, introns (noncoding nucleotide sequences) are excised from the primary transcript through processes known as editing and splicing. The result of these processes is a functional strand of mRNA. For most genes this is a routine step in the production of mRNA, but in some genes there are multiple ways to splice the primary transcript, resulting in different mRNAs, which in turn result in different proteins. Some genes also are controlled at the translational and posttranslational levels.

Mutations occur when the number or order of bases in a gene is disrupted. Nucleotides can be deleted, doubled, rearranged, or replaced, each alteration having a particular effect. Mutation generally has little or no effect, but, when it does alter an organism, the change may be lethal or cause disease. A beneficial mutation will rise in frequency within a population until it becomes the norm.

For more information on the influence of genetic mutations in humans and other organisms, see human genetic disease and evolution.

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Gene | Definition, Structure, Expression, & Facts | Britannica

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New gene therapy delivers treatment directly to brain

Posted: at 8:18 pm

When Rylae-Ann Poulin was a year old, she didnt crawl or babble like other kids her age. A rare genetic disorder kept her from even lifting her head. Her parents took turns holding her upright at night just so she could breathe comfortably and sleep.

Then, months later. doctors delivered gene therapy directly to her brain.

Now the 4-year-old is walking, running, swimming, reading and riding horses just doing so many amazing things that doctors once said were impossible, said her mother, Judy Wei.

READ MORE: Gene therapy was a boys last chance to stop leukemia. And it worked.

Rylae-Ann, who lives with her family in Bangkok, was among the first to benefit from a new way of delivering gene therapy attacking diseases inside the brain that experts believe holds great promise for treating a host of brain disorders.

Her treatment recently became the first brain-delivered gene therapy after its approval in Europe and the United Kingdom for AADC deficiency, a disorder that interferes with the way cells in the nervous system communicate. New Jersey drugmaker PTC Therapeutics plans to seek U.S. approval this year.

Meanwhile, about 30 U.S. studies testing gene therapy to the brain for various disorders are ongoing, according to the National Institutes of Health. One, led by Dr. Krystof Bankiewicz at Ohio State University, also targets AADC deficiency. Others test treatments for disorders such as Alzheimers, Parkinsons and Huntingtons.

Challenges remain, especially with diseases caused by more than a single gene. But scientists say the evidence supporting this approach is mounting opening a new frontier in the fight against disorders afflicting our most complex and mysterious organ.

Theres a lot of exciting times ahead of us, said Bankiewicz, a neurosurgeon. Were seeing some breakthroughs.

The most dramatic of those breakthroughs involve Rylae-Anns disease, which is caused by mutations in a gene needed for an enzyme that helps make neurotransmitters like dopamine and serotonin, the bodys chemical messengers. The one-time treatment delivers a working version of the gene.

At around 3 months old, Rylae-Ann began having spells her parents thought were seizures her eyes would roll back and her muscles would tense. Fluid sometimes got into her lungs after feedings, sending her to the emergency room. Doctors thought she might have epilepsy or cerebral palsy.

Around that time, Weis brother sent her a Facebook post about a child in Taiwan with AADC deficiency. The extremely rare disorder afflicts about 135 children worldwide, many in that country. Wei, who was born in Taiwan, and her husband, Richard Poulin III, sought out a doctor there who correctly diagnosed Rylae-Ann. They learned she could qualify for a gene therapy clinical trial in Taiwan.

Though they were nervous about the prospect of brain surgery, they realized she likely wouldnt live past 4 years old without it.

WATCH: Researchers look for link between air pollution and brain disease

Rylae-Ann had the treatment at 18 months old on November 13, 2019 which her parents have dubbed her reborn day. Doctors delivered it during minimally invasive surgery, with a thin tube through a hole in the skull. A harmless virus carried in a functioning version of the gene.

It gets put into the brain cells and then the brain cells make the (neurotransmitter) dopamine, said Stuart Peltz, CEO of PTC Therapeutics.

Company officials said all patients in their clinical trials showed motor and cognitive improvements. Some of them, Peltz said, could eventually stand and walk, and continue getting better over time.

Bankiewicz said all 40 or so patients in his teams NIH-funded study also saw significant improvements. His surgical approach is more involved and delivers the treatment to a different part of the brain. It targets relevant circuits in the brain, Bankiewicz said, like planting seeds that cause ivy to sprout and spread.

Its really amazing work, said Jill Morris, a program director with the National Institute of Neurological Disorders and Stroke, which helped pay for the research. And he has seen a lot of consistency between patients.

One is 8-year-old Rian Rodriguez-Pena, who lives with her family near Toronto. Rian got gene therapy in 2019, shortly before her 5th birthday. Two months later, she held her head up for the first time. She soon started using her hands and reaching for hugs. Seven months after surgery, she sat up on her own.

When the world was crumbling around us with COVID, we were at our house celebrating like it was the biggest party of our lives because Rian was just crushing so many milestones that were impossible for so long, said her mom, Shillann Rodriguez-Pena. Its a completely different life now.

Scientists say there are challenges to overcome before this approach becomes widespread for more common brain diseases.

For example, the timing of treatment is an issue. Generally, earlier in life is better because diseases can cause a cascade of problems over the years. Also, disorders with more complex causes like Alzheimers are tougher to treat with gene therapy.

When youre correcting one gene, you know exactly where the target is, said Morris.

Ryan Gilbert, a biomedical engineer at New Yorks Rensselaer Polytechnic Institute, said there can also be issues with the gene-carrying virus, which can potentially insert genetic information in an indiscriminate way. Gilbert and other researchers are working on other delivery methods, such as messenger RNA the technology used in many COVID-19 vaccines to deliver a genetic payload to the nucleus of cells.

Scientists are also exploring ways to deliver gene therapy to the brain without the dangers of brain surgery. But that requires getting around the blood-brain barrier, an inherent roadblock designed to keep viruses and other germs that may be circulating in the bloodstream out of the brain.

A more practical hurdle is cost. The price of gene therapies, borne mostly by insurers and governments, can run into the millions. The one-time PTC therapy, called Upstaza, costs more than $3 million in Europe, for example.

But drugmakers say they are committed to ensuring people get the treatments they need. And researchers are confident they can overcome the remaining scientific obstacles to this approach.

So I would say gene therapy can be leveraged for many sorts of brain diseases and disorders, Gilbert said. In the future, youre going to see more technology doing these kinds of things.

The families of Rylae-Ann and Rian said they hope other families dealing with devastating genetic diseases will someday get to see the transformations theyve seen. Both girls are continuing to improve. Rian is playing, eating all sorts of foods, learning to walk and working on language. Rylae-Ann is in preschool, has started a ballet class, and is reading at a kindergarten level.

When her dad picks her up, she runs to me just gives me a hug and says, I love you, Daddy. he said. Its like its a normal day, and thats all we ever wanted as parents.

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Indian Pharma Congress: Gene-cell therapy, preventive medicine future of health care, says expert – Economic Times

Posted: January 25, 2023 at 8:59 am

Indian Pharma Congress: Gene-cell therapy, preventive medicine future of health care, says expert  Economic Times

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A blood test that identifies people at higher risk of miscarriage? Thats the goal of this award-winning Rutgers med student. – The Philadelphia…

Posted: January 19, 2023 at 5:44 pm

A blood test that identifies people at higher risk of miscarriage? Thats the goal of this award-winning Rutgers med student.  The Philadelphia Inquirer

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Gene Therapy: Genes As Medicine | Pfizer

Posted: January 6, 2023 at 2:58 pm

References:

1. NIH Genetics Home Reference. What is a Gene? https://ghr.nlm.nih.gov/primer/basics/gene. Accessed February 10, 2020.

2. Forbes. How Many Possible Combinations of DNA Are There? https://www.forbes.com/sites/quora/2017/01/20/how-many-possible-combinations-of-dna-are-there/. Accessed February 10, 2020.

3. NIH National Human Genome Research Institute. Genetic Disorders. https://www.genome.gov/For-Patients-and-Families/Genetic-Disorders. Accessed February 10, 2020.

4. NIH Genetics Home Reference. How Can Gene Mutations Affect Health and Development? https://ghr.nlm.nih.gov/primer/mutationsanddisorders/mutationscausedisease. Accessed February 10, 2020.

5. NIH Genetics Home Reference. How does Gene Therapy Work? https://ghr.nlm.nih.gov/primer/therapy/procedures. Accessed February 10, 2020.

6. NIH Genetics Home Reference. What is Gene Therapy? https://ghr.nlm.nih.gov/primer/therapy/genetherapy. Accessed February 10, 2020.

7. Data on file. Pfizer Inc, New York, NY.

8. Haasteren J, Hyde S, Gill D. Lessons Learned From Lung and Liver In-Vivo Gene Therapy: Implications for the Future. Expert Opin Biol Ther. 2018;18(9):959-972.

9. Gowing G, Svendsen S, Svendsen CS. Ex Vivo Gene Therapy for the Treatment of Neurological Disorders. Prog Brain Res. 2017;230:99-132.

10. NIH National Human Genome Research Institute. What is Genome Editing? https://www.genome.gov/about-genomics/policy-issues/what-is-Genome-Editing. Accessed February 10, 2020.

11. Carroll D. Genome Engineering with Zinc-Finger Nucleases. Genetics. 2011;188(4):773-782.

12. Unniyampurath U, Krishnan M, et al. RNA Interference in the Age of CRISPR: Will CRISPR Interfere with RNAi? Int J Mol Sci. 2016;17(3):291.

13. Your Genome. Facts: What is Gene Therapy? http://www.yourgenome.org/facts/what-isgene-therapy. Accessed February 10, 2020.

14. Arruda VR, Favaro P, Finn JD. Strategies to Modulate Immune Responses: A New Frontier for Gene Therapy. Mol Ther. 2009;17(9):14921503.

15. Mingozzi F, High KA. Immune responses to AAV vectors: overcoming barriers to successful gene therapy. Blood. 2013;122(1):23-36.

16. Payne J. Antibody and antigen tests. Patient Platform Limited Web site. https://patient.info/health/antibody-and-antigen-tests. Accessed February 10, 2020.

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How Genomics will ensure a risk-free and beneficial treatment for good health and well-being – The Financial Express

Posted: December 28, 2022 at 11:17 pm

How Genomics will ensure a risk-free and beneficial treatment for good health and well-being  The Financial Express

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Regenerative Medicine Advanced Therapy Designation | FDA

Posted: December 18, 2022 at 2:29 pm

As described in Section 3033 of the 21st Century Cures Act, a drug is eligible for regenerative medicine advanced therapy (RMAT) designation if:

Based on FDAs interpretation of Section 506(g) of the Federal Food, Drug, and Cosmetic Act (as added by Section 3033 of the 21st Century Cures Act), certain human gene therapies and xenogeneic cell products may also meet the definition of a regenerative medicine therapy. For more information on FDAs definition of regenerative medicine therapies, refer to the Guidance for Industry, Expedited Programs for Regenerative Medicine Therapies for Serious Conditions.

The request for RMAT designation must be made either concurrently with submission of an Investigational New Drug application (IND) or as an amendment to an existing IND. We will not grant a RMAT designation if an IND is on hold or is placed on hold during the designation review.

You may submit a request for RMAT designation to:

Food and Drug AdministrationCenter for Biologics Evaluation and ResearchOffice of Tissues and Advanced TherapiesDocument Control Center10903 New Hampshire AvenueWO71, G112Silver Spring, MD 20993-0002

If the RMAT designation request is submitted to your IND as an amendment, the cover letter should specify that the submission contains a REQUEST FOR REGENERATIVE MEDICINE ADVANCED THERAPY DESIGNATION in bold, uppercase letters. If the request is submitted with an initial IND, the cover letter should specify that the submission contains both an INITIAL INVESTIGATIONAL NEW DRUG SUBMISSION and REQUEST FOR REGENERATIVE MEDICINE ADVANCED THERAPY DESIGNATION in bold, upper case letters.

No later than 60 calendar days after receipt of the designation request, the Office of Tissues and Advanced Therapies (OTAT) will notify the sponsor as to whether RMAT designation has been granted. If OTAT determines that the RMAT designation request was incomplete or that the drug development program does not meet the criteria for RMAT designation, OTAT will include a written description of the rationale for such determination.

10/06/2021

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3576 – Gene ResultCXCL8 C-X-C motif chemokine ligand 8 [ (human)]

Posted: November 23, 2022 at 5:04 am

Envelope surface glycoprotein gp120 env HIV-1 CN54, JRFL, and Ada Env (gp120) upregulates IL-6, CCL2, CCL4, CXCL8, and IL-1b through TLR4 and CCR5 induction in monocyte derived macrophages and hepatic stellate cells because treatment with an anti-TLR4 antibody mitigated the response PubMed env HIV-1 JRFL Env (gp120) upregulates IL8 in ARPE-19 cells PubMed env HIV-1 ADA infection decreases production of CXCL8 (IL8), CCL2 (MCP-1), and IL6 at a basal level or after Fc receptor, complement receptor 3, or bacterial stimulation in primary human macrophages PubMed env HIV-1 IIIB Env (gp120) upregulates production of TNF (TNF-a), IL-17A, CCL2 (MCP1), CCL5 (RANTES), IL6, IL10, CXCL8 (IL8), CXCL1 (GRO-a), and CCL1 (I309) in stimulated monocyte derived macrophages PubMed env Interleukin 8 (IL-8) gene expression is enhanced in monocytes treated with HIV-1 gp120 PubMed env Curcumin, a potent and safe anti-inflammatory compound, inhibits HIV-1 gp120-mediated upregulation of the proinflammatory cytokines TNF-alpha and IL-6, and the chemokines IL-8, RANTES, and IP-10 in primary human genital epithelial cells PubMed env HIV-1 gp120 upregulates the expression of interleukin 8 (IL8) in human B cells PubMed env HIV-1 gp120 upregulates the expression of IL-6 and IL-8 via the p38 signaling pathway and the PI3K/Akt signaling pathway in astrocytes PubMed env The binding of soluble HIV-1 gp120 to TLR2 or TLR4 results in upregulation of the TNF-alpha and IL-8 production through NF-kappaB activation PubMed env HIV-1 gp120-mediated increases in IL-8 production in astrocytes are mediated through the NF-KappaB pathway PubMed env In endometrial epithelium-derived cells, gp120 from CCR5-tropic HIV-1 increases the release of monocytes/chemokines-attracting chemokines (IL-8 and GRO) and proinflammatory cytokines (TNF-beta and IL-1alpha) PubMed Envelope transmembrane glycoprotein gp41 env The binding of soluble TLR2 to HIV-1 MA, CA, or gp41 inhibits the nuclear translocation of NFKB p65 subunit and downregulates CXCL8 (IL-8) and CCR5 expression, leading to inhibition of HIV-1 infection in cells PubMed env Evidence suggests HIV CA (p24) binds TLR2 and blocks activation by HIV MA (p17) and/or gp41 BUT DOES NOT block activation via Pam3CSK4 suggesting that HIV manipulates innate immune signaling through a TLR2-dependent mechanism PubMed env Exposure of TZM-bl 2 cells to CA (p24) for 1h prior to HIV gp41 decreases CXCL8 (IL-8) production yet has little to no effect on the inhibition of Pam3CSK4 (a synthetic bacterial TLR2/1 ligand) production of CXCL8 (IL-8) PubMed env Exposure of human T cells to HIV gp41 increases extracellular CXCL8 (IL-8) levels but to a lesser extent than CA (p24) and gp41 PubMed env A synthetic peptide corresponding to the immunosuppressive domain (amino acids 574-592) of HIV-1 gp41 inhibits activation of PBMCs and upregulates the expression of IL-8 in peptide-treated PBMCs PubMed env The interaction between HIV-1 gp41 fusion peptide and lymphocyte membrane is blocked by interleukin-8 and abolished by pre-treating the cells with heparin sulfate (HS) PubMed Nef nef HIV-1 Nef induces IL6 and CXCL8 (IL8) expression in a PIK3-PKC dependent, AKT independent manner PubMed nef HIV-1 Nef induces IL6 and IL8 expression through the NF-kappaB pathway PubMed nef HIV-1 Nef treatment induces IL6 and IL8 production in SVGA cells and primary human fetal astrocytes PubMed nef HIV-1 Tat and Nef combination treatment induces release of both IL-6 and IL-8 in human mesenchymal stem cells PubMed nef HIV-1 Nef expression by immature human and macaque dendritic cells (DCs) upregulates IL-6, IL-12, TNF-alpha, CXCL8, CCL3, and CCL4 release, but without upregulating co-stimulatory and other molecules characteristic of mature DCs PubMed Pr55(Gag) gag MVA-gag induces a significant release of cytokines such as IL-2R, IL-6, IL-8, TNF-alpha, IFN-gamma, MCP-1, MIP-1alpha, MIP-1beta, and RANTES by the infected monocyte-derived dendritic cells in comparison with uninfected cells PubMed Tat tat HIV-1 Tat upregulates CXCL8 mRNA and protein expression in CRT-MG human astroglioma cells PubMed tat HIV-1 Tat upregulates (CXCL8) IL8 protein expression in human monocytes and monocyte-derived dendritic cells in a TLR4-CD14-MD2 dependent manner PubMed tat HIV-1 Tat and Nef combination treatment induces release of both IL-6 and IL-8 in human mesenchymal stem cells PubMed tat HIV-1 Tat-induced upregulation of IL-8 in a time-dependent manner involves NF-kappaB and AP-1 transcription factors, activation of the p38 MAPK beta subunit, and PI3K/Akt pathway in astrocytes PubMed tat HIV-1 Tat upregulates IL-8 expression in astrocytes, monocytes, monocyte derived macrophages, Jurkat T-cells, HeLa cells, and human brain endothelial cells, an effect that likely contributes to the immune dysregulation observed during HIV-1 infection PubMed tat HIV-1 Tat downregulates the expression of adiponectin protein and upregulates the expression of IL-6, IL-8, and MCP-1 proteins in human SGBS preadipocytes PubMed tat HIV-1 Tat protein upregulates expression of IL-6 and IL-8 in human breast cancer cells by an NF-kappaB-dependent pathway PubMed tat HIV-1 Tat upregulates IL-8 and VEGF production and release from polymorphonuclear leukocytes (PMNL), indicating that PMNL recruitment by Tat is linked to angiogenesis PubMed tat HIV-1 Tat upregulation of IL-8 is linked to the cell cycle and involves NF-kappa B, RelA, c-rel, and CREB-binding protein PubMed tat Upregulation of IL-8 by HIV-1 Tat is implicated in the pathogenesis of Kaposi's sarcoma PubMed tat HIV-1 Tat downregulates IL-8 expression in the Raji B-cell line, however in the presence of PMA+PHA Tat induced IL-8 expression PubMed tat Upregulation of IL-8 by HIV-1 Tat in astrocytes is inhibited by the MEK1/2 inhibitor UO126, indicating a role for MEK1/2 in Tat-mediated chemokine induction PubMed Vpr vpr Treatment of human primary astrocytes with HIV-1 Vpr upregulates secretion of IL6, CXCL8 (IL8), MCP-1, and MIF and downregulates secretion of serpin E1, a serine proteinase inhibitor (known as PAI-1) PubMed vpr HIV-1 Vpr downregulates the expression of IL8 in human monocyte-derived dendritic cells PubMed vpr HIV-1 Vpr induced upregulation of CXCL8 (IL8) involves PI3K/Akt mediated activation of NFKB1 (NF-kappa-B) in astrocytes PubMed vpr HIV-1 Vpr-mediated upregulation of CXCL8 (IL8) involves NFKB1 (NF-kappa-B) PubMed vpr HIV-1 Vpr enhances the secretion of CXCL8 (IL8) from human fetal astrocytes PubMed vpr HIV-1 Vpr upregulates the expression of CXCL8 (IL8) mRNA in human fetal astrocytes PubMed vpr HIV-1 Vpr upregulates the expression fo CXCL8 (IL8) mRNA in SVGA in a dose-dependent manner PubMed vpr HIV-1 Vpr upregulates the expression of CXCL8 (IL8) mRNA in SVGA astrocytes in a time dependent fashion PubMed vpr HIV-1 Vpr enhances the secretion of CXCL8 (IL8) from SVGA astrocytes in a time dependent fashion PubMed vpr HIV-1 involves the JUN (AP-1) transcription factor in the induction of CXCL8 (IL8) in astrocytes PubMed vpr HIV-1 Vpr involves the CEBPD (C/EBP-delta) transcription factor in the induction of CXCL8 (IL8) in astrocytes PubMed vpr Vpr-mediated upregulation of CXCL8 (IL8) involves MAPK8 (JnK-MAPK) in astrocytes PubMed vpr Vpr-mediated upregulation of CXCL8 (IL8) in astrocytes involves p38-MAPK11 (beta isoform of p38-MAPK) PubMed vpr HIV-1 Vpr regulates interleukin 8 (CXCL8 (IL8)) expression, with reports showing both up- and downregulation of CXCL8 (IL8) PubMed capsid gag CXCL8-induced upregulation of HIV-1 p24 levels and 2-LTR circles is inhibited by CXCR1 or CXCR2 neutralization in HIV-1-infected monocytes-derived macrophages PubMed gag The binding of soluble TLR2 to HIV-1 MA, CA, or gp41 inhibits the nuclear translocation of NFKB p65 subunit and downregulates CXCL8 (IL-8) and CCR5 expression, leading to inhibition of HIV-1 infection in cells PubMed gag Treatment with chemokine CXCL8 significantly upregulates HIV-1 CA (p24) levels in supernatants of both HIV-1-infected monocytes-derived macrophages as well as microglia in a dose-dependent manner PubMed gag Evidence suggests HIV CA (p24) binds TLR2 and blocks activation by HIV MA (p17) and/or gp41 BUT DOES NOT block activation via Pam3CSK4 suggesting that HIV manipulates innate immune signaling through a TLR2-dependent mechanism PubMed gag Simultaneous exposure of TZM-bl2 cells with HIV CA(p24) and MA (p17) decreases MA (p17)- induced production of CXCL8 (IL-8) in a dose-dependent manner PubMed gag Exposure of TZM-bl 2 cells to CA(p24) for 1h prior to HIV gp41 or MA (p17) decreases CXCL8 (IL-8) production yet has little to no effect on the inhibition of Pam3CSK4 (a synthetic bacterial TLR2/1 ligand) production of CXCL8 (IL-8) PubMed gag Exposure of human T cells to HIV CA (p24) increases extracellular CXCL8 (IL-8) levels in a dose dependent manner and to a greater extent than gp41 but to a lesser extent than MA (p17) exposures. PubMed gag PLA-p24-loaded human monocyte-derived dendritic cells enhance the secretion of MIP-1beta, IL-6, IL-8, and TNF-alpha in comparison with PLA-loaded cells alone PubMed integrase gag-pol The formation of 2-long terminal repeat circles, a measure of viral genome integration, is higher in CXCL8-treated, HIV-1-infected monocytes-derived macrophages and microglia, suggesting the interaction between HIV-1 IN and CXCL8 PubMed gag-pol IL-8 decreases HIV-1 reverse transcription and viral integration during the early infection, suggesting the interaction between HIV-1 IN and IL-8 PubMed matrix gag Evidence suggests HIV CA (p24) binds TLR2 and blocks activation by HIV MA (p17) and/or gp41 BUT DOES NOT block activation via Pam3CSK4 suggesting that HIV manipulates innate immune signaling through a TLR2-dependent mechanism PubMed gag Simultaneous exposure of TZM-bl2 cells with HIV CA(p24) and MA (p17) decreases MA (p17)- induced production of CXCL8 (IL-8) in a dose-dependent manner PubMed gag Exposure of TZM-bl 2 cells to CA(p24) for 1h prior to HIV MA(p17) decreases CXCL8 (IL-8) production yet has little to no effect on the inhibition of Pam3CSK4 (a synthetic bacterial TLR2/1 ligand) production of CXCL8 (IL-8) PubMed gag Exposure of human T cells to HIV MA (p17) increases extracellular CXCL8 (IL-8) levels in a dose dependent manner and to a greater extent than CA (p24) and gp41. PubMed gag The binding of soluble TLR2 to HIV-1 MA, CA, or gp41 inhibits the nuclear translocation of NFKB p65 subunit and downregulates IL-8 and CCR5 expression, leading to inhibition of HIV-1 infection in cells PubMed gag Surface plasmon resonance analysis reveals that HIV-1 p17 binds IL-8 PubMed nucleocapsid gag HIV-1 NC upregulates IL8 in HEK 293T cells PubMed reverse transcriptase gag-pol IL-8 decreases HIV-1 reverse transcription and viral integration during the early infection, suggesting the interaction between HIV-1 RT and IL-8 PubMed

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3576 - Gene ResultCXCL8 C-X-C motif chemokine ligand 8 [ (human)]

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