The Homeodomain Resource is a searchable, curated collection of information for the homeodomain protein family. The resource is organized in a compact form and provides user-friendly interfaces for both querying the component databases and assembling customized datasets. The current release (version 5.0, October 2002) contains 1056 full-length homeodomain-containing sequences, 37 experimentally-derived structures, 81 homeodomain interactions, 84 homeodomain DNA-binding sites and 114 homeodomain proteins implicated in human genetic disorders. A new feature of this new release is the inclusion of experimentally-derived protein-protein interaction data for homeodomain family members. All entries are cross-linked for easy retrieval of the original records from source databases. The Homeodomain Resource is freely available through the World Wide Web at http://research.nhgri.nih.gov/homeodomain/.
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http://dx.doi.org/10.1093/nar/gkg118 | DOI Listing |
Nat Commun
January 2025
State Key Laboratory of Bioactive Substance and Function of Natural Medicines, NHC Key Laboratory of Biotechnology of Antibiotics, Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Acute myeloid leukemia (AML) featuring retinoic acid receptor-gamma (RARG) rearrangements exhibits morphological features resembling those of acute promyelocytic leukemia but is associated with drug resistance and poor clinical outcomes. However, the mechanisms underlying the role of RARG fusions in leukemogenesis remain elusive. Here, we show that RARG fusions disrupt myeloid differentiation and promote proliferation and self-renewal of hematopoietic stem and progenitor cells (HSPCs) by upregulating BCL2 and ATF3.
View Article and Find Full Text PDFPlant Sci
December 2024
State Key Laboratory of Subtropical Silviculture, Zhejiang A&F University, Hangzhou 311300, China; Zhejiang Provincial Key Laboratory of Resources Protection and Innovation of Traditional Chinese Medicine, Zhejiang A&F University, Hangzhou 311300, China. Electronic address:
EMBO J
January 2025
Neural Regeneration Lab, Neural Circuit Research Group, Korea Brain Research Institute, Daegu, Republic of Korea.
Neural stem cells (NSCs) can give rise to both neurons and glia, but the regulatory mechanisms governing their differentiation transitions remain incompletely understood. Here, we address the role of cyclin-dependent kinase inhibitors (CDKIs) in the later stages of dorsal cortical development. We find that the CDKIs p18 and p27 are upregulated at the onset of astrocyte generation.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
November 2024
Department of General Surgery, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, 570311 Haikou, Hainan, China.
Background: Emerging evidence indicates the essential role of cancer stem cells (CSCs) in the development and progression of various cancers, including colorectal cancer (CRC). CELF6, a member of the cytosine-uridine-guanine-binding protein (CUG-BP), Elav-like family (CELF), has been reported to be downregulated in CRC tissues. This study aims to elucidate the role and underlying mechanisms of CELF6 in CRC progression.
View Article and Find Full Text PDFNat Commun
November 2024
Department of Biological Repositories, Frontier Science Center for Immunology and Metabolism, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, 430071, China.
Human genetics analysis has identified many noncoding SNPs associated with diabetic traits, but whether and how these variants contribute to diabetes is largely unknown. Here, we focus on a noncoding variant, rs6048205, and report that the risk-G variant impairs the generation of PDX1+/NKX6-1+ pancreatic progenitor cells and further results in the abnormal decrease of functional β cells during pancreatic differentiation. Mechanistically, this risk-G variant greatly enhances RXRA binding and over-activates FOXA2 transcription, specifically in the pancreatic progenitor stage, which in turn represses NKX6-1 expression.
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