Person:
Halu, Arda

Profile Picture

Email Address

AA Acceptance Date

Birth Date

Research Projects

Organizational Units

Job Title

Last Name

Halu

First Name

Arda

Name

Halu, Arda
Author's Publications: search.filters.isAuthorOfPublication.b3c6ed22-8384-4b96-b43c-dc884b2c1212

Search Results

Now showing 1 - 2 of 2
  • Thumbnail Image
    Publication
    A Systems Approach to Refine Disease Taxonomy by Integrating Phenotypic and Molecular Networks
    (Elsevier, 2018) Zhou, Xuezhong; Lei, Lei; Liu, Jun; Halu, Arda; Zhang, Yingying; Li, Bing; Guo, Zhili; Liu, Guangming; Sun, Changkai; Loscalzo, Joseph; Sharma, Amitabh; Wang, Zhong
    The International Classification of Diseases (ICD) relies on clinical features and lags behind the current understanding of the molecular specificity of disease pathobiology, necessitating approaches that incorporate growing biomedical data for classifying diseases to meet the needs of precision medicine. Our analysis revealed that the heterogeneous molecular diversity of disease chapters and the blurred boundary between disease categories in ICD should be further investigated. Here, we propose a new classification of diseases (NCD) by developing an algorithm that predicts the additional categories of a disease by integrating multiple networks consisting of disease phenotypes and their molecular profiles. With statistical validations from phenotype-genotype associations and interactome networks, we demonstrate that NCD improves disease specificity owing to its overlapping categories and polyhierarchical structure. Furthermore, NCD captures the molecular diversity of diseases and defines clearer boundaries in terms of both phenotypic similarity and molecular associations, establishing a rational strategy to reform disease taxonomy.
  • Thumbnail Image
    Publication
    PARP9 and PARP14 cross-regulate macrophage activation via STAT1 ADP-ribosylation
    (Nature Publishing Group, 2016) Iwata, Hiroshi; Goettsch, Claudia; Sharma, Amitabh; Ricchiuto, Piero; Goh, Wilson Wen Bin; Halu, Arda; Yamada, Iwao; Yoshida, Hideo; Hara, Takuya; Wei, Mei; Inoue, Noriyuki; Fukuda, Daiju; Mojcher, Alexander; Mattson, Peter C.; Barabasi, Albert-Laszlo; Boothby, Mark; Aikawa, Elena; Singh, Sasha; Aikawa, Masanori
    Despite the global impact of macrophage activation in vascular disease, the underlying mechanisms remain obscure. Here we show, with global proteomic analysis of macrophage cell lines treated with either IFNγ or IL-4, that PARP9 and PARP14 regulate macrophage activation. In primary macrophages, PARP9 and PARP14 have opposing roles in macrophage activation. PARP14 silencing induces pro-inflammatory genes and STAT1 phosphorylation in M(IFNγ) cells, whereas it suppresses anti-inflammatory gene expression and STAT6 phosphorylation in M(IL-4) cells. PARP9 silencing suppresses pro-inflammatory genes and STAT1 phosphorylation in M(IFNγ) cells. PARP14 induces ADP-ribosylation of STAT1, which is suppressed by PARP9. Mutations at these ADP-ribosylation sites lead to increased phosphorylation. Network analysis links PARP9–PARP14 with human coronary artery disease. PARP14 deficiency in haematopoietic cells accelerates the development and inflammatory burden of acute and chronic arterial lesions in mice. These findings suggest that PARP9 and PARP14 cross-regulate macrophage activation.