Anti_Mouse_Human Timeless (Tim1) Antiserum 1
- Known as:
- Anti_Mouse_Human Timeless (Tim1) Antiserum 1
- Catalog number:
- TIM11/12-S
- Product Quantity:
- 100 ul
- Category:
- -
- Supplier:
- Alpha Dia
- Gene target:
- Anti_Mouse_Human Timeless (Tim1) Antiserum 1
Related genes to: Anti_Mouse_Human Timeless (Tim1) Antiserum 1
- Gene:
- DNAJC19 NIH gene
- Name:
- DnaJ heat shock protein family (Hsp40) member C19
- Previous symbol:
- -
- Synonyms:
- TIMM14, Tim14, Pam18
- Chromosome:
- 3q26.33
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-28
- Date modifiied:
- 2019-04-23
- Gene:
- PAM16 NIH gene
- Name:
- presequence translocase associated motor 16
- Previous symbol:
- -
- Synonyms:
- Magmas, Tim16, TIMM16
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2010-09-01
- Date modifiied:
- 2017-08-08
- Gene:
- TIMELESS NIH gene
- Name:
- timeless circadian regulator
- Previous symbol:
- -
- Synonyms:
- hTIM, TIM, TIM1
- Chromosome:
- 12q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-08
- Date modifiied:
- 2017-10-02
- Gene:
- TIMM13 NIH gene
- Name:
- translocase of inner mitochondrial membrane 13
- Previous symbol:
- TIMM13B
- Synonyms:
- Tim13
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-01
- Date modifiied:
- 2016-02-29
Related products to: Anti_Mouse_Human Timeless (Tim1) Antiserum 1
Related articles to: Anti_Mouse_Human Timeless (Tim1) Antiserum 1
- Major Depressive Disorder (MDD) has emerged as a leading cause of disability worldwide, affecting over 264 million people. Recent evidence reveals that disruption of circadian rhythms may be fundamental to MDD pathophysiology, opening new avenues for therapeutic intervention. - Source: PubMed
Publication date: 2026/06/03
Saeed SaboorSang RuiqiZhixin LimWang HuaizhiXu LeZhang XuhongHu Shaohua - Biological timing spans multiple scales, from second-to-minute behavioral decisions to daily rhythms and seasonally adjusted physiological states. Here, we use Drosophila clock genes as a model of gene co-option and functional modularity, asking how conserved circadian components are redeployed across diverse behavioral and physiological timescales. This review synthesizes current evidence on how core clock genes, including period (per), timeless (tim), Clock (Clk), and cycle (cyc), contribute not only to circadian rhythmicity but also to sleep regulation, developmental and reproductive timing, feeding and metabolic homeostasis, seasonal dormancy-related responses, and interval timing-like mating duration behaviors. Across these domains, clock-gene functions are shaped by cellular context, circuit architecture, transcriptional feedback, post-transcriptional and post-translational regulation, and environmental inputs such as light, temperature, nutrition, and social experience. Rather than treating these timing phenomena as isolated processes, we argue that they can be understood as examples of modular reuse of conserved molecular components. By centering the review on Drosophila and referring to mammalian studies only as comparative context where relevant, we highlight how clock-gene systems can be adapted to regulate behavior across biological timescales. - Source: PubMed
Publication date: 2026/06/01
Miao HongyuKim Woo Jae - Arsenic poisoning significantly elevates the risk of cancer and other chronic illnesses. The goal of this research is to identify important genes whose expression changes in response to arsenic toxicity, and the molecular pathways affected by arsenic, using computational analysis of arsenic toxicity profiles. This approach will computationally identify and analyze genes whose expression changes in response to arsenic, thereby elucidating the heightened risk of carcinogenesis in arsenic-exposed individuals. This work employed high-throughput arsenic toxicity profiles to computationally identify and analyze expressed genes (DEGs) differentially in Affymetrix microarray datasets from the Gene Expression Omnibus (GEO) database, which were screened using the GEO2R program. A protein-protein interaction (PPI) network was constructed using STRING to elucidate the functional links between these DEGs and DNA repair genes. Interactions between the seven central genes (E2F1, EXO1, EZH2, FEN1, HIST1H3A, POLA1, and TIMELESS) and the repair genes PARP1, NBN, PMS1, MSH3, XRCC5, XRCC6, MGMT, and MLH1 were discovered. We employed the DAVID and Enrichr-KG platforms to investigate the functions of these genes and their associations with cellular and molecular processes in greater detail. Two hundred eighty-one non-synonymous single-nucleotide polymorphisms (nsSNPs) in the 07 genes linked to arsenic toxicity were found using the COSMIC database. Based on our analysis, mutations in E2F1, EXO1, EZH2, FEN1, HIST1H3A, POLA1, and TIMELESS can hinder DNA repair mechanisms, ultimately leading to cancer. Our computational analysis demonstrated that these non-synonymous SNPs can affect gene function, potentially altering protein stability and activity. Furthermore, according to Metal-Protein docking and protein-protein docking, these genes and their mutations appear to affect interactions with repair proteins substantially. Specific dietary consumption may lessen the detrimental effects of arsenic poisoning on protein function. We hypothesized that the mutations might be reversed by attaching particular molecules to these mutants. The protective effects of six curcumin compounds were examined using molecular docking with AutoDock 4.2.6 to assess protein dynamics and binding interactions. Optimal complexes were selected for dynamics simulation using GROMACS, and potential strategies for long-term cancer prevention related to arsenic exposure were identified. - Source: PubMed
Parida LuckyPatel Trupti N - The expansion of prescribing authority to nurses is no longer debated on safety grounds. But a quieter anxiety remains: does prescribing change what nursing is? This paper uses Herbert Simon's The Sciences of the Artificial (1996) to move beyond the stalemate between two narratives: prescribing as rational adaptation to systemic complexity, or as defensive flight from the devaluation of relational work. Simon's concepts of inner and outer environment, satisficing and artefacts allow us to see the prescription as a human-made tool. Its impact on professional identity depends on how well nursing's inner environment, comprising its knowledge, values and relational logic, is designed into the act. The paper makes three claims. First, diagnostic authority, rather than prescribing itself, is the deeper boundary crossing. Second, the rational-defensive binary can be resolved with four contingency criteria: systemic demand, role clarity, relational proximity and educational design. Third, there is no timeless nursing essence to protect; prescribing is an artefact, and its effects are a matter of design, not destiny. The paper ends with a focused research agenda, practical implications and an invitation to treat the prescription pad as a test of whether nursing will prescribe as nursing or as something else. - Source: PubMed
Seguro José MiguelNeves Hugo - Five score years ago, Mr. Po-ling Chang, founder of Nankai University in China, established its timeless motto: "Dedication to Public Interests, Acquisition of All-Round Capability, and Aspiration for Progress with Each Passing Day." Today, Gui-Geng Liu, an alumnus of the 2017 Physics Po-ling Program (named after the founder of Nankai University, Mr. Po-ling Chang), has made groundbreaking contributions to topological physics, including the realization of the first three-dimensional Chern insulator and the photonic axion insulator. He is currently an independent Principal Investigator (PI) and doctoral supervisor at the School of Engineering, Westlake University. He has published in top-tier international journals, including Nature, Physical Review Letters, and Science. His research was recognized as one of the Top 10 Social Impact Events in China's Optics in 2022. In this edition of "Light People", I am pleased to feature Professor Gui-Geng Liu as he shares his personal journey and growth in the field. - Source: PubMed
Publication date: 2026/05/26
Wang Ji