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Critical Reviews™ in Immunology

Publicado 6 números por año

ISSN Imprimir: 1040-8401

ISSN En Línea: 2162-6472

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 1.3 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.6 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00079 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.24 SJR: 0.429 SNIP: 0.287 CiteScore™:: 2.7 H-Index: 81

Indexed in

Role of the Leucine Zipper Domain of CCAAT/ Enhancer Binding Protein-Epsilon (C/EBPε) in Neutrophil-Specific Granule Deficiency

Volumen 36, Edición 4, 2016, pp. 349-358
DOI: 10.1615/CritRevImmunol.2017019385
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SINOPSIS

Neutrophil-specific granule deficiency (SGD) is a rare autosomal recessive primary immunodeficiency characterized by bilobed neutrophil nuclei and lack of neutrophil-specific granule proteins such as lactoferrin. A deficiency of a myeloid-specific transcription factor, CCAAT/enhancer binding protein-epsilon (C/EBPε), has been identified as a cause of SGD. C/EBPε binds to DNA though its basic leucine zipper (bZIP) domain, and regulates terminal differentiation of neutrophils and expression of specific granule genes. Homozygous frameshift mutations resulting in loss of the bZIP domain have been reported in two patients with SGD. A recent observation showed that a homozygous 2-aa deletion in the bZIP domain with normal DNA-binding and dimerization abilities causes SGD by impairing protein−protein interactions with other transcription factors, indicating that multiple molecular mechanisms can lead to SGD. Studies of patient-derived mutations and analysis of C/EBPε knockout mice have shown the importance of the bZIP domain for the essential functions of C/EBPε.

CITADO POR
  1. Li Kening, Du Yuxin, Wei Dong-Qing, Zhang Fang, CEBPE expression is an independent prognostic factor for acute myeloid leukemia, Journal of Translational Medicine, 17, 1, 2019. Crossref

  2. Muraoka Masahiro, Akagi Tadayuki, Ueda Atsushi, Wada Taizo, Koeffler H. Phillip, Yokota Takashi, Yachie Akihiro, C/EBPε ΔRS derived from a neutrophil-specific granule deficiency patient interacts with HDAC1 and its dysfunction is restored by trichostatin A, Biochemical and Biophysical Research Communications, 516, 1, 2019. Crossref

  3. Liu Jin, Weiling Gu, Xueqin Li, Liang Xie, Linhong Wang, Zhongwen Chen, The CEBPE rs2239633 genetic polymorphism on susceptibility to childhood acute lymphoblastic leukemia: an updated meta-analysis, Environmental Health and Preventive Medicine, 26, 1, 2021. Crossref

  4. Banday Aaqib Zaffar, Kaur Anit, Akagi Tadayuki, Bhattarai Dharmagat, Muraoka Masahiro, Dev Diksha, Das Jhumki, Sachdeva Man Updesh Singh, Karmakar Indrani, Arora Kanika, Kaur Gurjit, Pandiarajan Vignesh, Jindal Ankur Kumar, Wada Taizo, Koeffler H. Phillip, Suri Deepti, Ahluwalia Jasmina, Kanegane Hirokazu, Bhatia Prateek, Rawat Amit, Singh Surjit, A Novel CEBPE Variant Causes Severe Infections and Profound Neutropenia, Journal of Clinical Immunology, 2022. Crossref

  5. Cheng Chi-Keung, Chan Hoi-Yun, Yung Yuk-Lin, Wan Thomas S. K., Leung Alex W. K., Li Chi-Kong, Tian Ke, Chan Natalie P. H., Cheung Joyce S., Ng Margaret H. L., A novel NUP98-JADE2 fusion in a patient with acute myeloid leukemia resembling acute promyelocytic leukemia, Blood Advances, 6, 2, 2022. Crossref

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