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https://www.readbyqxmd.com/read/29775011/-hyper-ige-syndromes
#1
REVIEW
Y Y He, B Liu, X P Xiao
A hyper-IgE syndrome is a rare immunodeficiesncy disease, often accompanied by high serum IgE. It often characterized by facial features, repeated skin infections, eczema and pulmonary infection, including autosomal dominant HIES (AD-HIES) and autosomal recessive HIES (AR-HIES). AR-HIES is caused by mutations in STAT3, which is presented as connective tissue, bone, vascular disease, and high brain white matter signal. AD-HIES is mainly caused by mutations in DOCK8 and TYK2, which is presented as severe viral infection and poor prognosis...
June 5, 2017: Journal of Clinical Otorhinolaryngology, Head, and Neck Surgery
https://www.readbyqxmd.com/read/29589523/an-update-on-jak-inhibitors
#2
Francesca Musumeci, Chiara Greco, Ilaria Giacchell, Anna Lucia Fallacara, Munjed M Ibrahim, Giancarlo Grossi, Chiara Brullo, Silvia Schenone
Janus kinases (JAKs) are a family of non-receptor tyrosine kinases, composed by four members, JAK1, JAK2, JAK3 and TYK2. JAKs are involved in different inflammatory and autoimmune diseases, as well as in malignancies, through the activation of the JAK/STAT signalling pathway. Furthermore, the V617F mutation in JAK2 was identified in patients affected by myeloproliferative neoplasms. This knowledge prompted researchers from academia and pharmaceutical companies to investigate this field in order to discover small molecule JAK inhibitors...
March 26, 2018: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/29157973/when-the-good-go-bad-mutant-npm1-in-acute-myeloid-leukemia
#3
REVIEW
Preethi Kunchala, Sudhakiranmayi Kuravi, Roy Jensen, Joseph McGuirk, Ramesh Balusu
Nucleophosmin 1 (NPM1) is a nucleolar phosphoprotein that performs diverse biological functions including molecular chaperoning, ribosome biogenesis, DNA repair, and genome stability. Acute myeloid leukemia (AML) is a heterogeneous disease, more than half of the AML cases exhibit normal karyotype (NK). Approximately 50-60 percent of patients with NK-AML carry NPM1 mutations which are characterized by cytoplasmic dislocation of the NPM1 protein. In AML, mutant NPM1 (NPM1c+) acts in a dominant negative fashion and also blocks the differentiation of myeloid cells through gain-of-function for the AML phenotype...
November 4, 2017: Blood Reviews
https://www.readbyqxmd.com/read/28184222/canonical-and-non-canonical-aspects-of-jak-stat-signaling-lessons-from-interferons-for-cytokine-responses
#4
REVIEW
Andrea Majoros, Ekaterini Platanitis, Elisabeth Kernbauer-Hölzl, Felix Rosebrock, Mathias Müller, Thomas Decker
Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signal transduction mediates cytokine responses. Canonical signaling is based on STAT tyrosine phosphorylation by activated JAKs. Downstream of interferon (IFN) receptors, activated JAKs cause the formation of the transcription factors IFN-stimulated gene factor 3 (ISGF3), a heterotrimer of STAT1, STAT2 and interferon regulatory factor 9 (IRF9) subunits, and gamma interferon-activated factor (GAF), a STAT1 homodimer. In recent years, several deviations from this paradigm were reported...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/27774824/inhibitors-of-jak-family-kinases-an-update-on-the-patent-literature-2013-2015-part-1
#5
REVIEW
Jason G Kettle, Annika Åstrand, Matthew Catley, Neil P Grimster, Magnus Nilsson, Qibin Su, Richard Woessner
Janus kinases (JAKs) are a family of four enzymes; JAK1, JAK2, JAK3 and tyrosine kinase 2 (TYK2) that are critical in cytokine signalling and are strongly linked to both cancer and inflammatory diseases. There are currently two launched JAK inhibitors for the treatment of human conditions: tofacitinib for Rheumatoid arthritis (RA) and ruxolitinib for myeloproliferative neoplasms including intermediate or high risk myelofibrosis and polycythemia vera. Areas covered: This review covers patents claiming activity against one or more JAK family members in the period 2013-2015 inclusive, and covers 95 patents from 42 applicants, split over two parts...
February 2017: Expert Opinion on Therapeutic Patents
https://www.readbyqxmd.com/read/27774822/inhibitors-of-jak-family-kinases-an-update-on-the-patent-literature-2013-2015-part-2
#6
REVIEW
Jason G Kettle, Annika Åstrand, Matthew Catley, Neil P Grimster, Magnus Nilsson, Qibin Su, Richard Woessner
Janus kinases (JAKs) are a family of four enzymes; JAK1, JAK2, JAK3 and tyrosine kinase 2 (TYK2) that are critical in cytokine signalling and are strongly linked to both cancer and inflammatory diseases. There are currently two launched JAK inhibitors for the treatment of human conditions: tofacitinib for Rheumatoid arthritis (RA) and ruxolitinib for myeloproliferative neoplasms including intermediate or high risk myelofibrosis and polycythemia vera. Areas covered: This review covers patents claiming activity against one or more JAK family members in the period 2013-2015 inclusive, and covers 95 patents from 42 applicants, split over two parts...
February 2017: Expert Opinion on Therapeutic Patents
https://www.readbyqxmd.com/read/27160622/-genetics-and-genomics-in-rheumatoid-arthritis-ra-an-update
#7
REVIEW
Ana Karen Rodríguez-Elías, Karina Maldonado-Murillo, Luis Fernando López-Mendoza, Julián Ramírez-Bello
Rheumatoid arthritis is a chronic inflammatory autoimmune disease that affects approximately 0.5-1% of the general population and leads to chronic synovial inflammation, destruction of cartilage and bone, and disability. The heritability of rheumatoid arthritis has been estimated to be about 60%, while the contribution of HLA to heritability has been estimated to be 11-37%. Other genes, such as PTPN22, STAT4, CTLA4, TRAF1, PADI4, IRF5, FCRL3, TNFIP3, TNF-α, miRNAs, CD28, CD40, TYK2, etc., have been associated with susceptibility, severity, activity, and treatment response of rheumatoid arthritis...
March 2016: Gaceta Médica de México
https://www.readbyqxmd.com/read/27020257/viral-infections-in-type-1-diabetes-mellitus-why-the-%C3%AE-cells
#8
REVIEW
Anne Op de Beeck, Decio L Eizirik
Type 1 diabetes mellitus (T1DM) is caused by progressive autoimmune-mediated loss of pancreatic β-cell mass via apoptosis. The onset of T1DM depends on environmental factors that interact with predisposing genes to induce an autoimmune assault against β cells. Epidemiological, clinical and pathology studies in humans support viral infection--particularly by enteroviruses (for example, coxsackievirus)--as an environmental trigger for the development of T1DM. Many candidate genes for T1DM, such as MDA5, PTPN2 and TYK2, regulate antiviral responses in both β cells and the immune system...
May 2016: Nature Reviews. Endocrinology
https://www.readbyqxmd.com/read/26780035/interactions-of-the-immune-system-with-skin-and-bone-tissue-in-psoriatic-arthritis-a-comprehensive-review
#9
REVIEW
Andrea Sukhov, Iannis E Adamopoulos, Emanual Maverakis
Cutaneous psoriasis (e.g., psoriasis vulgaris (PsV)) and psoriatic arthritis (PsA) are complex heterogeneous diseases thought to have similar pathophysiology. The soluble and cellular mediators of these closely related diseases are being elucidated through genetic approaches such as genome-wide association studies (GWAS), as well as animal and molecular models. Novel therapeutics targeting these mediators (IL-12, IL-23, IL-17, IL-17 receptor, TNF) are effective in treating both the skin and joint manifestations of psoriasis, reaffirming the shared pathophysiology of PsV and PsA...
August 2016: Clinical Reviews in Allergy & Immunology
https://www.readbyqxmd.com/read/26631911/tyrosine-kinase-2-surveillant-of-tumours-and-bona-fide-oncogene
#10
REVIEW
Nicole R Leitner, Agnieszka Witalisz-Siepracka, Birgit Strobl, Mathias Müller
Tyrosine kinase 2 (TYK2) is a member of the Janus kinase (JAK) family, which transduces cytokine and growth factor signalling. Analysis of TYK2 loss-of-function revealed its important role in immunity to infection, (auto-) immunity and (auto-) inflammation. TYK2-deficient patients unravelled high similarity between mice and men with respect to cellular signalling functions and basic immunology. Genome-wide association studies link TYK2 to several autoimmune and inflammatory diseases as well as carcinogenesis...
January 2017: Cytokine
https://www.readbyqxmd.com/read/26215033/the-immunogenetics-of-psoriasis-a-comprehensive-review
#11
REVIEW
Jamie L Harden, James G Krueger, Anne M Bowcock
Psoriasis vulgaris is a common, chronic inflammatory skin disease with a complex etiology involving genetic risk factors and environmental triggers. Here we describe the many known genetic predispositions of psoriasis with respect to immune genes and their encoded pathways in psoriasis susceptibility. These genes span an array of functions that involve antigen presentation (HLA-Cw6, ERAP1, ERAP2, MICA), the IL-23 axis (IL12Bp40, IL23Ap19, IL23R, JAK2, TYK2), T-cell development and T-cells polarization (RUNX1, RUNX3, STAT3, TAGAP, IL4, IL13), innate immunity (CARD14, c-REL, TRAF3IP2, DDX58, IFIH1), and negative regulators of immune responses (TNIP1, TNFAIP3, NFKBIA, ZC3H12C, IL36RN, SOCS1)...
November 2015: Journal of Autoimmunity
https://www.readbyqxmd.com/read/25970001/primary-immunodeficiencies-with-elevated-ige
#12
REVIEW
Trine H Mogensen
In recent years a number of primary immunodeficiencies (PIDs) characterized by elevated Immunoglobulin E (IgE) levels have been uncovered and termed as Hyper-IgE syndrome (HIES). In addition to the elevated levels of IgE, patients with these PIDs display a spectrum of infections by staphylococci and fungi, and in some cases viruses, particularly affecting skin and lungs. Most of these PIDs also have a non-infectious phenotype, comprising musculoskeletal, vascular, and neurological abnormalities. The genetic basis for the majority of conditions with elevated IgE has now been established and includes mutations in STAT3, DOCK8, TYK2, and most recently PGM3 molecules...
2016: International Reviews of Immunology
https://www.readbyqxmd.com/read/25488777/genetics-of-psoriatic-arthritis
#13
REVIEW
Darren D O'Rielly, Proton Rahman
Spondyloarthritis (SpA) represents a group of inflammatory rheumatic diseases that cluster within families and possess overlapping clinical features. The pathogenesis of SpA encompasses a complex array of genetic, immunological and environmental factors. In this article, we will briefly review the genetics of PsA, and then focus on the genes that may be potentially linked either directly or indirectly to the immunopathology of the Th-17 pathway. The most consistent and dominant genetic effect of PsV and PsA is located on chromosome 6p21...
October 2014: Best Practice & Research. Clinical Rheumatology
https://www.readbyqxmd.com/read/25291316/toward-selective-tyk2-inhibitors-as-therapeutic-agents-for-the-treatment-of-inflammatory-diseases
#14
Christel J Menet
The family of JAK comprises four members and has received significant attention in recent years from the pharmaceutical industry as a therapeutic target. The role of JAK is central to cytokine signaling pathways. It is believed that selective modulation of one specific JAK can lead to the inhibition of a restricted set of cytokines, which should avoid undesired side effects and get closer to the profile of biologic therapies. Consequently, selective JAK inhibition has become a major focus area of drug discovery research...
July 2014: Pharmaceutical Patent Analyst
https://www.readbyqxmd.com/read/25057888/the-molecular-regulation-of-janus-kinase-jak-activation
#15
REVIEW
Jeffrey J Babon, Isabelle S Lucet, James M Murphy, Nicos A Nicola, Leila N Varghese
The JAK (Janus kinase) family members serve essential roles as the intracellular signalling effectors of cytokine receptors. This family, comprising JAK1, JAK2, JAK3 and TYK2 (tyrosine kinase 2), was first described more than 20 years ago, but the complexities underlying their activation, regulation and pleiotropic signalling functions are still being explored. Here, we review the current knowledge of their physiological functions and the causative role of activating and inactivating JAK mutations in human diseases, including haemopoietic malignancies, immunodeficiency and inflammatory diseases...
August 15, 2014: Biochemical Journal
https://www.readbyqxmd.com/read/24654603/therapeutic-potential-of-tyrosine-kinase-2-in-autoimmunity
#16
REVIEW
Yan Liang, Yan Zhu, Yi Xia, Hui Peng, Xiao-Ke Yang, Yan-Yan Liu, Wang-Dong Xu, Hai-Feng Pan, Dong-Qing Ye
INTRODUCTION: Tyrosine kinase 2 (Tyk2) is a Janus kinase family member that is crucial for signaling transduction in response to a wide variety of cytokines, including type I IFNs, IL-6, IL-10, IL-12 and IL-23. An appropriate expression of Tyk2-mediated signaling might be essential for maintaining normal immune responses. AREAS COVERED: This review summarizes that Tyk2 is essential for the differentiation and function of a wide variety of immune cells, including natural killer cells, B cells, as well as T helper cells...
May 2014: Expert Opinion on Therapeutic Targets
https://www.readbyqxmd.com/read/24252238/dysregulation-of-jak-stat-pathway-in-hematological-malignancies-and-jak-inhibitors-for-clinical-application
#17
Muhammad Furqan, Nikhil Mukhi, Byung Lee, Delong Liu
JAK-STAT (Janus associated kinase-signal transducer and activator of transcription) pathway plays a critical role in transduction of extracellular signals from cytokines and growth factors involved in hematopoiesis, immune regulation, fertility, lactation, growth and embryogenesis. JAK family contains four cytoplasmic tyrosine kinases, JAK1-3 and Tyk2. Seven STAT proteins have been identified in human cells, STAT1-6, including STAT5a and STAT5b. Negative regulators of JAK-STAT pathways include tyrosine phosphatases (SHP1 and 2, CD45), protein inhibitors of activated STATs (PIAS), suppressors of cytokine signaling (SOCS) proteins, and cytokine-inducible SH2-containing protein (CIS)...
January 16, 2013: Biomarker Research
https://www.readbyqxmd.com/read/23384668/advances-in-the-discovery-of-selective-jak-inhibitors
#18
Christel J Menet, Luc Van Rompaey, Raphaël Geney
In this review, we describe the current knowledge of the biology of the JAKs. The JAK family comprises the four nonreceptor tyrosine kinases JAK1, JAK2, JAK3, and Tyk2, all key players in the signal transduction from cytokine receptors to transcription factor activation. We also review the progresses made towards the optimization of JAK inhibitors and the importance of their selectivity profile. Indeed, the full array of many medicinal chemistry enabling tools (HTS, X-ray crystallography, scaffold morphing, etc...
2013: Progress in Medicinal Chemistry
https://www.readbyqxmd.com/read/23367873/inhibitors-of-jak2-and-jak3-an-update-on-the-patent-literature-2010-2012
#19
REVIEW
Brian W Dymock, Cheng Shang See
INTRODUCTION: Janus kinases (JAKs) comprise a family of four enzymes, JAK1, JAK2, JAK3 and tyrosine kinase 2 (TYK2), centrally implicated in cell signaling processes important in cancer and immune-inflammatory diseases. Progression in the field has taken a recent step forward with the approval of ruxolitinib (Jakafi), a selective inhibitor of JAK1/2 and very recently tofacitinib (Xeljanz), a pan-JAK inhibitor. There are many new JAK family enzyme inhibitors in the clinic now with a range of selectivity profiles...
April 2013: Expert Opinion on Therapeutic Patents
https://www.readbyqxmd.com/read/22971156/selective-jak1-inhibitor-and-selective-tyk2-inhibitor-patents
#20
REVIEW
Peter Norman
INTRODUCTION: The JAK family comprises of the four non-receptor tyrosine kinases JAK1, JAK2, JAK3 and Tyk2, which play key, but differing, roles in cytokine receptor signal transduction. A non-selective JAK inhibitor, ruxolitinib, has recently been approved to treat myelofibrosis whereas tofacitinib is poised for approval to treat rheumatoid arthritis. Selective inhibition of JAK3, JAK1 or Tyk2 provides the opportunity to achieve clinical efficacy in the treatment of inflammatory diseases while reducing the risk of dose-limiting effects attributable to JAK2 inhibition...
October 2012: Expert Opinion on Therapeutic Patents
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