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Line 1: {{Short description\|Toxin from snake}} {{Orphan\|date=July 2024}} [[Toxin]] '''BF9''' is a [[Kunitz domain\|Kunitz-type peptide]], coming from snakes, with a dual functionality. The toxin is able to inhibit both [[serine protease]]s and [[potassium channel]]s (more specifically the [[KCNA3\|K<sub>v</sub>1.3 channel]]). == Etymology and source == Venom basic protease inhibitor IX, also named BF9, is derived from the venom of the elapid snake ''[[Banded krait\|Bungarus fasciatus]]''. The ‘BF’ in the name originates from the snake's [[nomenclature]]. This Kunitz-type peptide is the first functionally characterized snake toxin that inhibits both [[protease~~\|proteases~~]]s and potassium channels.<ref name=":0">{{Cite journal \|last1=Yang \|first1=Weishan \|last2=Feng \|first2=Jing \|last3=Wang \|first3=Bin \|last4=Cao \|first4=Zhijian \|last5=Li \|first5=Wenxin \|last6=Wu \|first6=Yingliang \|last7=Chen \|first7=Zongyun \|date=2013-11-14 \|title=BF9, the First Functionally Characterized Snake Toxin Peptide with Kunitz-Type Protease and Potassium Channel Inhibiting Properties: KUNITZ-TYPE PROTEASE AND POTASSIUM CHANNEL INHIBITOR FROM SNAKE \|url=https://onlinelibrary.wiley.com/doi/10.1002/jbt.21538 \|journal=Journal of Biochemical and Molecular Toxicology \|language=en \|volume=28 \|issue=2 \|pages=76–83 \|doi=10.1002/jbt.21538\|pmid=24243656 \|s2cid=1493475 }}</ref> == Chemistry == Line 19 ⟶ 20: K<sub>v</sub>1.3 channels are among others expressed in [[T cell\|T-cells]].<ref name=":2">{{Cite journal \|last1=Beeton \|first1=Christine \|last2=Wulff \|first2=Heike \|last3=Standifer \|first3=Nathan E. \|last4=Azam \|first4=Philippe \|last5=Mullen \|first5=Katherine M. \|last6=Pennington \|first6=Michael W. \|last7=Kolski-Andreaco \|first7=Aaron \|last8=Wei \|first8=Eric \|last9=Grino \|first9=Alexandra \|last10=Counts \|first10=Debra R. \|last11=Wang \|first11=Ping H. \|last12=LeeHealey \|first12=Christine J. \|last13=S. Andrews \|first13=Brian \|last14=Sankaranarayanan \|first14=Ananthakrishnan \|last15=Homerick \|first15=Daniel \|date=2006-11-14 \|title=Kv1.3 channels are a therapeutic target for T cell-mediated autoimmune diseases \|journal=Proceedings of the National Academy of Sciences \|volume=103 \|issue=46 \|pages=17414–17419 \|doi=10.1073/pnas.0605136103 \|pmid=17088564 \|pmc=1859943 \|bibcode=2006PNAS..10317414B \|issn=0027-8424 \|doi-access=free }}</ref> Therefore, if these channels are inhibited, the [[Memory T cell\|effector-memory T-cells]] are affected.<ref name=":2" /> The overexpression of K<sub>v</sub>1.3 channels in T-cells can lead to [[~~Autoimmune~~autoimmune disease~~\|autoimmune diseases~~]]s,<ref name=":2" /> and a higher level of [[~~Factor~~factor XI~~\|factor XIa~~]]a can lead to [[thrombosis]].<ref>{{Cite journal \|last1=Wu \|first1=Wenman \|last2=Li \|first2=Hongbo \|last3=Navaneetham \|first3=Duraiswamy \|last4=Reichenbach \|first4=Zachary W. \|last5=Tuma \|first5=Ronald F. \|last6=Walsh \|first6=Peter N. \|date=2012-07-19 \|title=The kunitz protease inhibitor domain of protease nexin-2 inhibits factor XIa and murine carotid artery and middle cerebral artery thrombosis \|url=http://dx.doi.org/10.1182/blood-2012-03-419523 \|journal=Blood \|volume=120 \|issue=3 \|pages=671–677 \|doi=10.1182/blood-2012-03-419523 \|pmid=22674803 \|pmc=3401218 \|issn=0006-4971}}</ref> Using its properties, BF9 can potentially be used as a treatment drug that targets the K<sub>v</sub>1.3 channels and the XIa coregulation factor.<ref name=":1" /> == References ==

BF9: Difference between revisions