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Coagulation factor IX

FIX, coagulation factor IX, Christmas factor
This gene encodes vitamin K-dependent coagulation factor IX that circulates in the blood as an inactive zymogen. This factor is converted to an active form by factor XIa, which excises the activation peptide and thus generates a heavy chain and a light chain held together by one or more disulfide bonds. The role of this activated factor IX in the blood coagulation cascade is to activate factor X to its active form through interactions with Ca+2 ions, membrane phospholipids, and factor VIII. Alterations of this gene, including point mutations, insertions and deletions, cause factor IX deficiency, which is a recessive X-linked disorder, also called hemophilia B or Christmas disease. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: FVIII, CAN, HAD, FX, FXI
Papers using FIX antibodies
Lymphoid enhancer factor 1 directs hair follicle patterning and epithelial cell fate
Coulombe Pierre A. et al., In The Journal of Cell Biology, 1994
... Materials were obtained from the following sources: 129SvJ mouse genomic library packaged into Lambda Fix II and pBluescript vector from Stratagene (La Jolla, CA); restriction endonucleases and DNA modifying enzymes from New England Biolabs ...
Finding Groups in Data: An Introduction to Cluster Analysis.
Unutmaz Derya, In PLoS ONE, 1989
... with FACS staining buffer (BD Pharmingen, San Diego, USA) and fixed with 1 ml of 1× Fix/Perm buffer (Biolegend, San Diego, CA, USA ...
Papers on FIX
Long acting recombinant coagulation factor IX albumin fusion protein (rIX-FP) in hemophilia B: results of a phase 3 trial.
Jacobs et al., Milano, Italy. In Blood, Feb 2016
UNASSIGNED: A global Phase 3 study evaluated the pharmacokinetics, efficacy and safety of recombinant fusion protein linking coagulation factor IX with albumin (rIX-FP) in 63 previously treated male patients (12-61 years) with severe hemophilia B (FIX activity ≤ 2%).
New products for the treatment of haemophilia.
Laffan, London, United Kingdom. In Br J Haematol, Jan 2016
First amongst these are modified Factor VIII (FVIII) and Factor IX (FIX) molecules with extended half-lives.
In Vitro Mode of Action and Anti-thrombotic Activity of Boophilin, a Multifunctional Kunitz Protease Inhibitor from the Midgut of a Tick Vector of Babesiosis, Rhipicephalus microplus.
Francischetti et al., Bethesda, United States. In Plos Negl Trop Dis, Jan 2016
Notably, we also identified Boophilin as a non-competitive inhibitor of FXIa, preventing FIX activation.
Distinct X chromosomal rearrangements in four haemophilia B patients with entire F9 deletion.
Kojima et al., Nagoya, Japan. In Haemophilia, Jan 2016
INTRODUCTION: Haemophilia B is an X-linked bleeding disorder caused by a coagulation factor IX gene (F9) abnormality.
Low-dose continuous infusion of factor VIII in patients with haemophilia A.
Kitanovski et al., Ljubljana, Slovenia. In Blood Transfus, Dec 2015
BACKGROUND: Patients with haemophilia A (HA) or B (HB) can be given prophylactic or on-demand treatment administered by continuous infusion or bolus injections of factor VIII (FVIII) or IX (FIX).
Approaches for recombinant human factor IX production in serum-free suspension cultures.
Swiech et al., Ribeirão Preto, Brazil. In Biotechnol Lett, Dec 2015
OBJECTIVE: To establish a serum-free suspension process for production of recombinant human factor IX (rhFIX) based on the human cell line HEK 293T by evaluating two approaches: (1) serum-free suspension adaptation of previously genetic modified cells (293T-FIX); and (2) genetic modification of cells already adapted to such conditions (293T/SF-FIX).
In vivo induction of regulatory T cells for immune tolerance in hemophilia.
Herzog et al., Gainesville, United States. In Cell Immunol, Nov 2015
While formation of inhibitors directed against factor IX, FIX, resulting from hemophilia B treatment is comparatively rare, a serious complication that is often associated with additional immunotoxicities, e.g.
Health-related quality of life assessment in haemophilia patients on prophylaxis therapy: a systematic review of results from prospective clinical trials.
Valentino et al., Cambridge, United States. In Haemophilia, Sep 2015
METHODS: We performed a systematic literature review of clinical trials evaluating the efficacy of prophylaxis with factor VIII, FIX or bypassing agents.
New and Emerging Agents for the Treatment of Hemophilia: Focus on Extended Half-Life Recombinant Clotting Proteins.
Ragni, Pittsburgh, United States. In Drugs, Sep 2015
Hemophilia A and B are X-linked disorders caused by deficient or defective clotting factor VIII (FVIII) or IX factor (FIX) proteins, and characterized by spontaneous or traumatic bleeding into joints and muscles.
Mesenchymal stem cell treatment for hemophilia: a review of current knowledge.
Mazza et al., Brussels, Belgium. In J Thromb Haemost, Jun 2015
In contrast, the sustained production of endogenous factors VIII (FVIII) or IX (FIX) by the patient's own cells could represent a curative treatment.
An RNAi therapeutic targeting antithrombin to rebalance the coagulation system and promote hemostasis in hemophilia.
Akinc et al., Cambridge, United States. In Nat Med, May 2015
Hemophilia A and B are inherited bleeding disorders characterized by deficiencies in procoagulant factor VIII (FVIII) or factor IX (FIX), respectively.
Promoterless gene targeting without nucleases ameliorates haemophilia B in mice.
Kay et al., Stanford, United States. In Nature, Feb 2015
In particular, we target a promoterless human coagulation factor IX (F9) gene to the liver-expressed mouse albumin (Alb) locus.
Population pharmacokinetics of plasma-derived factor IX in adult patients with haemophilia B: implications for dosing in prophylaxis.
Ahlén et al., Uppsala, Sweden. In Eur J Clin Pharmacol, 2012
The disposition of FIX was well described by a three-compartment PK model.
Spectrum of F9 mutations in Chinese haemophilia B patients: identification of 20 novel mutations.
Fu et al., Shanghai, China. In Pathology, 2012
The F9 mutations were heterogenous and the missense mutations were the most prevalent gene defects in Chinese haemophilia B patients.
Factor IX mutations in haemophilia B patients in Malaysia: a preliminary study.
Ayob et al., Kuala Lumpur, Malaysia. In Malays J Pathol, 2012
factor IX mutations were identified in either the exon or intronic regions in haemophilia B patients in Malaysia; one novel mutation, 6660_6664delTTCTT was identified in siblings with moderate form of haemophilia B
Productive recognition of factor IX by factor XIa exosites requires disulfide linkage between heavy and light chains of factor XIa.
Walsh et al., Philadelphia, United States. In J Biol Chem, 2012
Partial reduction of FXIa/S557A to produce heavy and light chains resulted in decreased FIX binding, and this function was regained upon reformation of the disulfide linkage between the heavy and the light chains.
Adenovirus-associated virus vector-mediated gene transfer in hemophilia B.
Davidoff et al., London, United Kingdom. In N Engl J Med, 2012
METHODS: We infused a single dose of a serotype-8-pseudotyped, self-complementary adenovirus-associated virus (AAV) vector expressing a codon-optimized human factor IX (FIX) transgene (scAAV2/8-LP1-hFIXco) in a peripheral vein in six patients with severe hemophilia B (FIX activity, <1% of normal values).
Development of inhibitors in haemophilia. Ongoing epidemiological study.
Schramm et al., Timişoara / Temesvár, Romania. In Hamostaseologie, 2011
A number of 513 consecutive patients (494-haemophilia A and 19-haemophilia B) from eight haemophilia treatment centers have been investigated with Bethesda assay for the presence of factor VIII or IX inhibitors.
Host plant genome overcomes the lack of a bacterial gene for symbiotic nitrogen fixation.
Suganuma et al., Tsukuba, Japan. In Nature, 2009
A Fix(-) (non-fixing) plant mutant, fen1, forms morphologically normal but ineffective nodules.
Genotype analysis identifies the cause of the "royal disease".
Moliaka et al., Worcester, United States. In Science, 2009
The mutation occurs in F9, a gene on the X chromosome that encodes blood coagulation factor IX, and is predicted to alter RNA splicing and to lead to production of a truncated form of factor IX. Thus, the royal disease is the severe form of hemophilia, also known as hemophilia B or Christmas disease.
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