MDM2 Antibody
- Known as:
- MDM2 Antibody
- Catalog number:
- abx000690
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- MDM2 Antibody
Related genes to: MDM2 Antibody
- Gene:
- MDM2 NIH gene
- Name:
- MDM2 proto-oncogene
- Previous symbol:
- -
- Synonyms:
- HDM2, MGC5370
- Chromosome:
- 12q15
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-10
- Date modifiied:
- 2017-12-01
Related products to: MDM2 Antibody
Related articles to: MDM2 Antibody
- Dedifferentiated liposarcoma (DDLPS) may originate in perihepatic adipose tissue, but can radiologically present as a hepatic mass. Moreover, dense Immunoglobulin G4 (IgG4)-positive plasma cell infiltration may mimic IgG4-related disease (IgG4-RD) and delay curative-intent resection. We herein describe a unique case that exemplifies this diagnostic pitfall. - Source: PubMed
Publication date: 2026/05/07
Shibusawa SoushiYamashita YukiTanaka TomoyukiKimura TakefumiSano ShuseiTamada HisashiOka YusukeOzawa YoshikiMori HiromitsuWada Shuichi - Necroptosis is a form of programmed cell death that promotes tumor immunogenicity. To identify druggable regulators of necroptosis, we performed a small-molecule inhibitor screen and identified mouse double minute 2 (MDM2) as a suppressor of tumor necrosis factor α (TNF-α)-induced necroptosis. Genetic deletion or pharmacologic inhibition of MDM2 markedly enhanced necroptosis in a receptor-interacting protein kinase 1 (RIPK1)-dependent and p53-independent manner. Mechanistically, MDM2 interacted with RIPK3 and promoted its proteasome-mediated degradation, thereby limiting RIPK3 abundance and restraining pathway activation. , MDM2 deficiency increased tumor cell necroptosis, promoted inflammatory remodeling of the tumor microenvironment (TME), and enhanced CD8 T cell infiltration, leading to improved tumor control. In immunologically "cold" tumor models, combining MDM2 inhibition with anti-PD-1 blockade converted tumors to a T cell-inflamed state and significantly improved therapeutic efficacy, even in p53-deficient settings. These findings identify MDM2 as a regulator of TNF-α-induced necroptosis and highlight its potential as a therapeutic target for cancer immunotherapy. - Source: PubMed
Publication date: 2026/04/11
Wu YingxinYu HanyangZhang ZongxuXiong WeihangZeng ZexianLiu WeiliTu HailinLin Xin - Ataxia-telangiectasia and Rad3-related (ATR) is an essential DNA damage response kinase that protects genome integrity by controlling cell cycle checkpoints, regulating origin firing, stabilizing replication forks, and signaling DNA repair. Due to hyper-proliferation, cancer cells depend on ATR for survival, implicating ATR inhibitors as promising therapeutics. However, variable tumor responses to ATR inhibitors highlights the need to uncover the determinants of cell fate. Here, we show breast cancer sensitivity to ATR inhibition correlates with the appearance of pan-nuclear DNA damage. The fate of these cells is driven by a p53-p21-RB1 axis that triggers a G2-to-G0-like cell cycle exit and is buffered by the p53 inhibitor MDM2. MDM2 inhibition lowers the DNA damage threshold for cell cycle exit and robustly targets ATR inhibitor-resistant cells. Our work reveals cell cycle plasticity as a mechanism determining cell fate during ATR inhibition and identifies MDM2 as a target for increasing ATR inhibitor efficacy. - Source: PubMed
Publication date: 2026/05/01
Sanchez CelinaMarmolejo Carlos OrigelLee JuyoungSaldivar Joshua C - The management of retroperitoneal well-differentiated liposarcoma (WDLPS) in elderly, surgically ineligible patients remains a therapeutic challenge. Eribulin, a microtubule inhibitor, has demonstrated activity in advanced non-WDLPS liposarcoma subtypes; however, its efficacy in pure well-differentiated liposarcoma (WDLPS) remains exploratory, and long-term outcomes in elderly patients are not well documented. - Source: PubMed
Publication date: 2026/04/21
Fan JiwenChen MeijingDai QunyaoCheng BoranLai WenjuanWang ShubinTong Gangling - Hepatocellular carcinoma (HCC) originates from damaged hepatocytes in chronic liver injury. Though HCC development requires oncoproteins-mediated p53 inhibition, both genetic deletion and continous activation of p53 specifically in mouse hepatocytes are shown to promote liver tumorigenesis, suggesting that chronic liver injury firstly activates p53, and p53 activity needs to be dynamically regulated for preventing hepatocarcinogenesis. Yet, it remains unaddressed how liver injury stresses trigger signaling pathways to rapidly activate p53 prior to its inactivation in a physiological setting. Two pathways, ribosomal proteins (RPs)-MDM2 and 14-3-3-MDMX, are shown to activate p53 upon stresses, and mutations of MDM2 or MDMX that may disrupt these pathways have been found in human cancers including HCC. Using our unique double knock-in (DKI) mice that contain wild-type p53 while harbor defects in these two pathways, we unveiled that basal level of p53 in DKI mice is sufficient for maintaining liver function, however, carcinogen- or unhealthy diet-induced HCC initiation is accelerated in DKI mice. The two p53-pathways are also activated in human cirrhotic livers. We futher identified a one-carbon metabolism (1CM) enzyme methylenetetrahydrofolate dehydrogenase 1 like (MTHFD1L) as the p53-suppressed player in HCC initiation. We found that MTHFD1L is upregulated in human early HCC and correlated with p53 status, and promotes mouse HCC initiation by enhancing autonomous growth and immune evasion of HCC initiating cells (HCICs). With Nanopore RNA-m A-sequencing, we unveiled that MTHFD1L fulfills these bi-functions by fueling methionine cycle that produces methyl groups to maintain the mRNA m A of Snail (an HCC early tumorigenesis driver) and B2m (a light chain of MHC-I required for antigen presentation to CD8+ T) in HCICs. Our findings demonstrate that the two stress-triggered p53-pathways are crucial for preventing liver early tumorigenesis by reversing MTHFD1L upregulation-associated 1CM reprogramming and subsequent Snail and B2m mRNA-m A-mediated cell autonomous growth and immune evasion. - Source: PubMed
Publication date: 2026/04/30
Lu HuaZhang Yi-WeiPeng GangLiao WenjuanJung Ji HoonLi CaiyueLiu YunlongGao HongZha YitianPham NathanMeaderis StephenEslter EvanZhang YanpingDhar DebanjanZeng Shelya