BIT1 Antibody
- Known as:
- BIT1 Antibody
- Catalog number:
- XW-7770
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- BIT1 Antibody
Related genes to: BIT1 Antibody
- Gene:
- PTRH2 NIH gene
- Name:
- peptidyl-tRNA hydrolase 2
- Previous symbol:
- -
- Synonyms:
- BIT1, CGI-147, PTH2, CFAP37
- Chromosome:
- 17q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-22
- Date modifiied:
- 2016-10-05
Related products to: BIT1 Antibody
Related articles to: BIT1 Antibody
- Acquired resistance to epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) remains a substantial clinical obstacle in treating lung adenocarcinoma (LUAD). Identifying pro-survival pathways that allow tumor cells to evade TKI-induced apoptosis is critical for overcoming this resistance. The transcriptional repressor transducin-like enhancer of split 1 (TLE1) was previously identified as a crucial oncogenic factor that promotes survival in resistant cells. This study investigates the mitochondrial protein Bcl-2 inhibitor of transcription 1 (Bit1) as a key pro-apoptotic signal that overrides the TLE1-mediated survival program. - Source: PubMed
Dela Cruz Ma CarmelaYao XinNealy AlajahBailey JamesNalls MicahMedina Paul MarkChen RenweiBiliran Hector - Mitochondrial dynamics, orchestrated by a finely tuned balance between fusion and fission, are critical for cellular homeostasis and development. Dysregulation of these processes has been increasingly implicated in various diseases, including developmental disorders. Although core components, such as mitofusin 1 and 2 (MFN1/2), have been characterized, the broader regulatory network remains incompletely defined. - Source: PubMed
Publication date: 2026/03/10
Na DoHyeongYoo SeungminJeong MuhahLee NahyunKim YoungwonKim YoubinCho Dong-HyungJung Yong-Keun - Prostate adenocarcinoma (PRAD) is a common malignancy in the male genitourinary system, with growing evidence linking its progression to mitochondrial function and macrophage polarization. This study identifies prognostic genes associated with these factors in PRAD through integrated transcriptomic data analysis and Mendelian randomization (MR). - Source: PubMed
Publication date: 2025/12/31
Heng LiBian HaoZhao ChengjunWei ZhenCao JianchengWang Guanfeng - Wooden breast (WB) is a prevalent meat quality defect in broilers, characterized by muscle hardness, and reduced functionality. To investigate its molecular basis, we applied an integrated multi-omics strategy combining untargeted metabolomics, proteomics, and phosphoproteomics. By integrating these datasets, our study offers more comprehensive understanding of the protein and signaling landscape in WB compared to previous approaches. Metabolomic showed an energy crisis marked by ATP depletion. Proteomic revealed downregulation of glycolytic, tricarboxylic acid cycle, and oxidative phosphorylation, indicating metabolic dysfunction. Machine learning identified five candidate biomarkers (GOLGA2, AHCYL2, L1CAM, PTRH2, GOLPH3). Phosphoproteomic analysis detected 4348 sites and highlighted RHOA/ROCK signaling pathway activation, suggesting roles in cytoskeletal remodeling and fibrosis. Integrated analyses revealed that WB is associated with impaired energy metabolism, calcium dysregulation, ER stress, and fibrotic progression. These findings provide mechanistic insights and identify potential molecular targets to improve meat quality and reduce economic losses. - Source: PubMed
Publication date: 2025/12/16
Ding CongRen MeijuanLi ZhixuanLiu ShiqiSun HaomingYu SijiaChen YiweiLi XingyuNiu QiangLi BingLi LiYang XiaojunSun Qingzhu - The peptidyl-tRNA hydrolase 2 (PTRH2, Bit-1, BIT1) gene plays a pro-survival role during development with loss of function gene mutations causing congenital infantile multisystem disease (IMNEPD). In wild-type female mice hearts, Ptrh2 protein levels significantly increase during pregnancy and decrease postpartum, demonstrating a protective role in response to pregnancy-initiated cardiac stresses. Peripartum cardiomyopathy (PPCM) is due to dysregulated protective signaling in the pregnant heart. The genetic and molecular mechanisms underlying PPCM remain poorly defined with no specific therapies. Here, we engineered a cardiac-specific Ptrh2 knockout (Ptrh2-CKO) mouse and show these maternal mice develop left ventricular systolic dysfunction, exhibit high rates of postpartum heart failure, and model key features of human PPCM. Infusion of a caspase 3-specific inhibitor attenuated the PPCM phenotype. Collectively, our findings demonstrate Ptrh2 is a negative regulator of pregnancy-induced cardiac stresses by activating pro-survival signals and blocking apoptotic signals, suggesting Ptrh2 may be a therapeutic target for the treatment of PPCM. - Source: PubMed
Publication date: 2025/12/19
Montoya-Uribe VanessaChoubey PoojaWalton Chad BGlibetic NatalijaSeok Yang WonAan Femke JLindsey SarahPeplowska KarolinaHernandez Brenda YRamos Joe WMatter Michelle L