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@ARTICLE{Zhang:179730,
      author       = {C. Zhang and H. He and J. Dai and Y. Li and J. He and W.
                      Yang and J. Dai and F. Han and W. Kong and X. Wang and X.
                      Zheng and J. Zhou and W. Pan and Z. Chen and S. Mahak$^*$
                      and Y. Zhang and F. Guo and J. Hu},
      title        = {{KANK}4 {P}romotes {A}rteriogenesis by {P}otentiating
                      {VEGFR}2 {S}ignaling in a {TALIN}-1-{D}ependent {M}anner.},
      journal      = {Arteriosclerosis, thrombosis, and vascular biology},
      volume       = {42},
      number       = {6},
      issn         = {0276-5047},
      address      = {Stanford, Calif.},
      publisher    = {HighWire},
      reportid     = {DKFZ-2022-00862},
      pages        = {772-788},
      year         = {2022},
      note         = {2022 Jun;42(6):772-788 / DKFZ-ZMBH Alliance},
      abstract     = {Arteriogenesis plays a critical role in maintaining
                      adequate tissue blood supply and is related to a favorable
                      prognosis in arterial occlusive diseases. Strategies aimed
                      at promoting arteriogenesis have thus far not been
                      successful because the factors involved in arteriogenesis
                      remain incompletely understood. Previous studies suggest
                      that evolutionarily conserved KANK4 (KN motif and ankyrin
                      repeat domain-containing proteins 4) might involve in
                      vertebrate vessel development. However, how the KANK4
                      regulates vessel function remains unknown. We aim to
                      determine the role of endothelial cell-specifically
                      expressed KANK4 in arteriogenesis.The role of KANK4 in
                      regulating arteriogenesis was evaluated using Kank4-/- and
                      KANK4iECOE mice. Molecular mechanisms underlying
                      KANK4-potentiated arteriogenesis were investigated by
                      employing RNA transcriptomic profiling and mass spectrometry
                      analysis.By analyzing Kank4-EGFP reporter mice, we showed
                      that KANK4 was specifically expressed in endothelial cells.
                      In particular, KANK4 displayed a dynamic expression pattern
                      from being ubiquitously expressed in all endothelial cells
                      of the developing vasculature to being explicitly expressed
                      in the endothelial cells of arterioles and arteries in
                      matured vessels. In vitro microfluidic chip-based vascular
                      morphology analysis and in vivo hindlimb ischemia assays
                      using Kank4-/- and KANK4iECOE mice demonstrated that
                      deletion of KANK4 impaired collateral artery growth and the
                      recovery of blood perfusion, whereas KANK4 overexpression
                      leads to increased vessel caliber and blood perfusion. Bulk
                      RNA sequencing and Co-immunoprecipitation/mass spectrometry
                      (Co-IP/MS) analysis identified that KANK4 promoted EC
                      proliferation and collateral artery remodeling through
                      coupling VEGFR2 (vascular endothelial growth factor receptor
                      2) to TALIN-1, which augmented the activation of the VEGFR2
                      signaling cascade.This study reveals a novel role for KANK4
                      in arteriogenesis in response to ischemia. KANK4 links
                      VEGFR2 to TALIN-1, resulting in enhanced VEGFR2 activation
                      and increased EC proliferation, highlighting that KANK4 is a
                      potential therapeutic target for promoting arteriogenesis
                      for arterial occlusive diseases.},
      keywords     = {arteriole (Other) / endothelial cell (Other) / hind limb
                      (Other) / mice (Other) / perfusion (Other)},
      cin          = {A190},
      ddc          = {610},
      cid          = {I:(DE-He78)A190-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35477278},
      doi          = {10.1161/ATVBAHA.122.317711},
      url          = {https://inrepo02.dkfz.de/record/179730},
}