Plasminogen activator

Function

Plasminogen activator (PLA) is a serine protease which converts plasminogen to plasmin. TPA structure contains heavy and light chains (HC, LC). PLA is inhibited by PLA inhibitor 1 and 2.

  • Tissue PLA (TPA) which is involved in breakdown of blood clots.
  • Urokinase-type PLA see Urokinase.
  • Coagulase/fibrinolysin is a plasminogen activator from Yersinia pestis which possesses coagulase activity is responsible for degradation of plasmid-coded outer membrane proteins[1].

Relevance

Treatment with tissue PLA for acute ischemic stroke is beneficial[2].

Structural highlights

  • . Water molecules are shown as red spheres.
  • .

Human tissue plasminogen activator light chain catalytic domain (sky blue and green), heavy chain catalytic domain fragment (yellow and pink) complex with benzamidine, 1a5h

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3D structures of plasminogen activator3D structures of plasminogen activator

Updated on 21-July-2024

  • Tissue plasminogen activator; Domains – fibrin-binding 36-85; kringle 1 69-153; kringle 2 209-298; catalytic 311-561
    • 1a5h – hTPA HC+LC + benzamidine – human
    • 1rtf - hTPA HC+LC
    • 1tpg – hTPA F1-G - NMR
    • 1pk2 – hTPA kringle 2 domain + 6-aminohexanoic acid – NMR
    • 1tpk, 1pml - hTPA kringle 2 domain
    • 1kdu - hTPA kringle 1 domain – NMR
    • 1tpm, 1tpn - hTPA fibrin-binding domain – NMR
    • 1bda – hTPA catalytic domain (mutant) + EGR-CMK
    • 5brr, 5zlz - hTPA catalytic domain (mutant) + plasminogen activator inhibitor 1
  • Coagulase/fibrinolysin
    • 2x55, 2x56 - YpTPA – Yersinia pestis
    • 2x4m - YpTPA (mutant)
    • 4dcb - YpTPA (mutant) + plasminogen peptide
  • Urokinase-type plasminogen activator see Urokinase

ReferencesReferences

  1. Sodeinde OA, Sample AK, Brubaker RR, Goguen JD. Plasminogen activator/coagulase gene of Yersinia pestis is responsible for degradation of plasmid-encoded outer membrane proteins. Infect Immun. 1988 Oct;56(10):2749-52. PMID:2843471
  2. . Tissue plasminogen activator for acute ischemic stroke. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. N Engl J Med. 1995 Dec 14;333(24):1581-7. PMID:7477192 doi:http://dx.doi.org/10.1056/NEJM199512143332401

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