PP2447 Blocking Peptide
- Known as:
- PP2447 Blocking Peptide
- Catalog number:
- 33r-5833
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- PP2447 Blocking Peptide
Related genes to: PP2447 Blocking Peptide
- Gene:
- TRABD NIH gene
- Name:
- TraB domain containing
- Previous symbol:
- -
- Synonyms:
- PP2447
- Chromosome:
- 22q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2006-07-06
- Date modifiied:
- 2014-11-19
Related products to: PP2447 Blocking Peptide
Related articles to: PP2447 Blocking Peptide
- The aim of this study was to investigate the mediating role of immune cells in the relationship between plasma proteins and the risk of major depressive disorder (MDD). Using a two-step, two-sample Mendelian randomization (MR) approach, we systematically assessed whether immune cells mediate the causal effects of plasma proteins on MDD. We found that eleven plasma proteins (TRABD, CACNB4, EDA, SAR1A, GLRX, COTL1, STOM, CRP, FGF22, and EDA2R) were positively associated with MDD risk, while one protein (SPTLC1) exhibited a negative association. Additionally, seven immune cell phenotypes-including CD14 on CD33dim HLA DR + CD11b + , memory B cells (% of B cells), IgD⁻ CD24⁻ % B cells, CD20 on B cells, CD27 on IgD⁺ CD24⁺, CD27 on IgD⁻ CD38dim, and CD62L on CD62L⁺ DCs-showed potential causal effects on MDD. Further mediation analysis revealed that three immune cell types mediated the effects of four plasma proteins on MDD: CD27 on IgD⁺ CD24⁺ cells mediated the effects of both COTL1 and RNF122 (mediation proportions: 5.13% and 4.50%, respectively); IgD⁻ CD24⁻ % B cells mediated the effect of EDA (12.1%); and CD62L on CD62L⁺ DCs mediated the effect of GLRX (-9.46%). The negative mediation proportion suggests a protective pathway. Sensitivity analyses supported the robustness of these findings.These results provide novel insights into immune-mediated mechanisms linking plasma proteins to MDD and may inform future research into targeted immunotherapeutic strategies. - Source: PubMed
Publication date: 2025/11/13
Jia RuolingNie MingkunWang XunYang Yang - Mitochondria serve as hubs for many critical cellular processes, and their functions and dynamics are tightly controlled. TRABD is a Tiki/TraB family protein with unknown function. Here, we characterized TRABD as a novel outer mitochondrial membrane protein. Depletion of in cells severely impairs mitochondrial respiration and ATP production, inhibits cell growth, increases reactive oxygen species levels. Depletion of also affects mitochondrial dynamics and mitophagy, possibly through interactions with PGAM5. Knockout of in mice significantly exacerbates ischemia reperfusion-induced renal tubular injury by promoting mitochondrial fragmentation and damage. Our study identified a novel outer mitochondrial membrane protein and revealed the critical roles of TRABD in mitochondrial dynamics and ischemia reperfusion-induced renal tubular injury. - Source: PubMed
Publication date: 2025/07/24
Duan WenqiWu WenyeYang CuiZhang MeiLi XuemeiTian WenminChen YangZhang Xinjun - The mitochondrial proteome arises from dual genetic origins. Nuclear-encoded proteins need to be transported across or inserted into two distinguished membranes, and the translocase of the outer mitochondrial membrane (TOM) complex represents the main translocase in the outer mitochondrial membrane. Its composition and regulation have been extensively investigated within yeast cells. However, we have little knowledge of the TOM complex composition within human cells. Here, we have defined the TOM interactome in a comprehensive manner using biochemical approaches to isolate the TOM complex in combination with quantitative mass spectrometry analyses. With these studies, we defined the pleiotropic nature of the human TOM complex, including new interactors, such as TRABD. Our studies provide a framework to understand the various biogenesis pathways that merge at the TOM complex within human cells. - Source: PubMed
Publication date: 2025/04/24
Özdemir MetinOeljeklaus SilkeSchendzielorz AlexanderMorgenstern MarcelValpadashi AnushaYousefi RoyaWarscheid BettinaDennerlein Sven - Triple negative breast cancer (TNBC) continues to be the most aggressive subtype of breast cancer that frequently develops resistance to chemotherapy. Doxorubicin (DOX) belongs to the anthracycline chemical class of the drug and is one of the widely used anticancer drugs. This study investigates the mechanism of m6A methyltransferase ZC3H13 in DOX resistance of TNBC. - Source: PubMed
Publication date: 2025/02/26
Huang LiHan LeiLiang ShuaiHan Guohui - High TRABD expression is associated with tau pathology in patients with Alzheimer's disease; however, the function of TRABD is unknown. Human TRABD encodes a mitochondrial outer-membrane protein. The loss of TRABD resulted in mitochondrial fragmentation, and TRABD overexpression led to mitochondrial clustering and fusion. The C-terminal tail of the TRABD anchored to the mitochondrial outer membrane and the TraB domain could form homocomplexes. Additionally, TRABD forms complexes with MFN2, MIGA2, and PLD6 to facilitate mitochondrial fusion. Flies lacking dTRABD are viable and have normal lifespans. However, aging flies exhibit reduced climbing ability and abnormal mitochondrial morphology in their muscles. The expression of dTRABD is increased in aged flies. dTRABD overexpression leads to neurodegeneration and enhances tau toxicity in fly eyes. The overexpression of dTRABD also increased reactive oxygen species (ROS), ATP production, and protein turnover in the mitochondria. This study suggested that TRABD-induced mitochondrial malfunctions contribute to age-related neurodegeneration. - Source: PubMed
Publication date: 2024/06/05
Zhou CaixiaLi ZhirongLi YawenLi YaoyaoWang WeiShang WeinaLiu Jun-PingWang LiquanTong Chao