TRIB2 antibody
- Known as:
- TRIB2 (anti-)
- Catalog number:
- orb100536
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- TRIB2 antibody
Related genes to: TRIB2 antibody
- Gene:
- TRIB2 NIH gene
- Name:
- tribbles pseudokinase 2
- Previous symbol:
- -
- Synonyms:
- TRB2, GS3955
- Chromosome:
- 2p24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-30
- Date modifiied:
- 2016-10-05
Related products to: TRIB2 antibody
Related articles to: TRIB2 antibody
- Second generation antiandrogens, such as enzalutamide, are commonly prescribed to treat advanced prostate cancer. However, enzalutamide resistant prostate cancer (ERPC) invariably develops with more aggressive features. Management of ERPC is extremely difficult not only because available therapies cannot effectively eliminate ERPC cells but also due to enhanced growth and highly metastatic features in ERPC cells to invade distant organs. This problem is amplified by the lack of proper knowledge about suitable molecular targets in ERPC cells. Recently, we reported that Tribbles 2 (TRIB2), is overexpressed in ERPC cells and tumors and inhibition of TRIB2 kills ERPC cells via apoptosis. TRIB2 enhances cancer cell growth and invasion and confers resistance to enzalutamide, while inhibition of TRIB2 resensitizes the resistant cells. Interestingly, TRIB2 induces neuroendocrine (NE) features in ERPC cells and both the and treatment-emergent NEPC cells consistently overexpress TRIB2. Though TRIB2 has emerged as a promising target, suitable inhibitors are not commercially available for clinical use. We used artificial intelligence (AI)-based molecular modeling to design a series of small chemical entities with potentially high specificity to bind with TRIB2. Extensive virtual screening and molecular editing yielded few highly selective and potent agents to inhibit TRIB2 and kill ERPC-NE/NEPC cells. One such compound (HF-125) directly binds to destabilize and degrade TRIB2 proteins involving proteasomes and is effective both and . Based on these findings, HF-125 emerges as a promising novel agent for development of a new therapeutic strategy for ERPC-NE/NEPC types of aggressive prostate cancer. - Source: PubMed
Publication date: 2026/04/30
Chowdhury Sougata GhoshBiswas PritamMonga JitenderBrown SteveRogers CraigGhosh Jagadananda - Cardiovascular disease (CVD) represents a significant global public health challenge, with its high incidence and mortality rates imposing a substantial socioeconomic burden. Tribbles family proteins (TRIB1, TRIB2, and TRIB3), functioning as pseudokinases, play a pivotal role in the pathogenesis and progression of various CVDs, including coronary heart disease, heart failure, hypertension, cardiomyopathy, and pulmonary hypertension. The progression of CVD is modulated by the tribbles family proteins through key mechanisms such as the regulation of inflammatory responses, apoptosis, endoplasmic reticulum stress, and insulin signaling pathways. Furthermore, polymorphisms within the tribbles family genes are strongly associated with genetic susceptibility to CVDs, thereby influencing disease risk and clinical manifestations. Multiple therapeutic strategies targeting the tribbles family have demonstrated potential in improving cardiac and vascular function, offering novel avenues for CVD treatment. This review provides an in-depth analysis of the structural characteristics of tribbles family proteins and elucidates the mechanisms of tribbles in CVDs and their potential as therapeutic targets. - Source: PubMed
Publication date: 2026/03/19
Zhang WenkangZhang MinhaoSha ZiqiYan GaoliangTang ChengchunLi Mingkang - The myeloid oncogene TRIB2 is a key driver of acute myeloid leukaemia (AML) pathogenesis, promoting chemoresistance and blocking differentiation through ubiquitin-mediated degradation of the C/EBPα transcription factor. Despite its stable and sometimes elevated expression across AML subtypes, TRIB2 remains a clinically untargeted vulnerability. Here, we present a comprehensive investigation into TRIB2 degradation mechanisms using multimodal approaches, including CRISPR knockout, mutational protein stability, small molecule TRIB2 engagement, and evaluation of a novel targeted protein degrader (TRIB2-PROTAC). We identify afatinib, a multi-ERBB covalent inhibitor, as a rapid inducer of TRIB2 degradation, triggering AML cell death potentially via signalling pathways distinct from ERBB. Importantly, TRIB2 degradation synergised with cytarabine, the frontline AML chemotherapy, amplifying therapeutic efficacy. Mapping of TRIB2 ubiquitination sites revealed Lys-63 as critical for its own proteolytic turnover, and a Lys-to-Arg degradation-resistant mutant (KallR) conferred enhanced chemoresistance and increased leukaemic engraftment in vivo. CRISPR-mediated TRIB2 knockout validated an essential role in AML cell survival. Consistently, the novel TRIB2-PROTAC (compound 5K) achieved robust TRIB2 degradation and AML cell killing at low micromolar concentrations. These findings establish TRIB2 as a compelling therapeutic target in AML and demonstrate that leveraging the ubiquitin-proteasome system to degrade TRIB2 offers a promising strategy to overcome chemoresistance. The present work provides strong preclinical rationale for the development of TRIB2-targeting therapies in AML. - Source: PubMed
Rigby EvieFasanella Masci FrancescaNarayanan AksharaKania ElzbietaHarris John AWilliams JamieZhang BinghuaLiu LijunRichmond LauraZhou FengtaoDing KeCarmody Ruaidhrí JEyers Patrick AKeeshan Karen - Hepatoblastoma (HB) is the most common pediatric liver malignancy with an increasing incidence. However, the functional roles of 3D chromatin organization, epigenetic regulatory factors, and transcriptional reprogramming in HB pathogenesis remain poorly understood. - Source: PubMed
Publication date: 2025/12/29
Wu HanZhu GuoqingZhu QianshuMa JiMao SiweiDing MiaoZhu JiabeiTang XiaochenBian ZhixuanShan YuhuaGu SongSun FenyongJiang CizhongPan Qiuhui - Metabolic dysfunction-associated steatohepatitis (MASH, previously NASH) is the severe type of metabolic dysfunction-associated steatotic liver disease (MASLD, previously NAFLD), the most common liver condition. The excessive hepatic lipid accumulation triggers apoptosis of hepatocytes and lobular inflammation, which are the key features of MASH. MASH may develop into liver fibrosis, while current therapeutics exhibit limited responses in patients. Identification of novel upstream regulators for both hepatic inflammation and fibrosis holds great promise to treat MASH and liver fibrosis. Pseudokinases, which contain the pseudokinase domains without kinase activity, are hub genes that integrate the signaling pathways of cell death, inflammation and fibrosis in the liver. We critically analyze the STAT and other signaling pathways through which JAK1, JAK2 (kinases with pseudokinase domains), TRIB2, MLKL and IRAK-M regulate the progression of MASH and liver fibrosis. Collectively, pseudokinases are potential therapeutic targets for treating MASH and liver fibrosis. Although the pseudokinase inhibitors show effectively treat inflammatory diseases, specific and safe pseudokinase inhibitors are understudied. Proteolysis targeting chimeras (PROTACs) are rapidly evolved bifunctional molecules that efficiently bind to and catalytically degrade the target proteins via recruiting E3 ubiquitin ligases. We discuss the design, selectivity, and limitations of pseudokinase PROTACs, and present the most active lead PROTACs that may treat MASH and liver fibrosis at distinct stages. Furthermore, innovative strategies enhance PROTACs' efficacy through addressing the main translational hurdles, especially the low bioavailability and cellular uptake. It facilitates the development of PROTACs to probe in vivo function of pseudokinases and to combat MASH and liver fibrosis. - Source: PubMed
Publication date: 2025/12/02
Wang YibingPeng Jiajing