Ask about this productRelated genes to: PDLIM2 antibody
- Gene:
- PDLIM2 NIH gene
- Name:
- PDZ and LIM domain 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 8p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-12-08
- Date modifiied:
- 2016-04-25
Related products to: PDLIM2 antibody
Related articles to: PDLIM2 antibody
- Bone tissue possesses strong regenerative potential, but large segmental bone defects often exceed its intrinsic capacity for self-healing. Human adipose-derived stem cells (hASCs) offer a promising cellular basis for bone regeneration owing to their robust osteogenic differentiation potential. However, the role of PDZ and LIM domain 2 (PDLIM2) play in hASC osteogenesis and its relationship with the Wnt/β-catenin signaling pathway remain poorly understood. - Source: PubMed
Shi YulianFan TingyuQu RongmeiWu GuoshengLi XiangtianLiu JiaxuanFeng ZiyiWu HaopengOuyang JunDai Jingxing - Benjakul (BJK) remedy, traditionally used to balance the four elements, has demonstrated clinical efficacy in relieving inflammation and allergic rhinitis (AR) symptoms. This study investigated differential serum peptide expression in AR patients treated with BJK remedy compared to loratadine using MALDI-TOF MS and LC-MS/MS. MALDI-TOF MS revealed four shared mass peptide patterns that were significantly upregulated ( < 0.05) after 3 and 6 weeks of both treatments. Identifying the peptides, 17β-hydroxysteroid dehydrogenase (17β-HSD) and microtubule-actin cross-linking factor 1 (MACF1) were linked to inflammatory suppression and hormonal balance, while zinc finger CCCH-type containing 4 (ZC3H4) and transducin beta-like protein 3 (TBL3) were associated with the relief of pulmonary fibrosis. Conversely, zinc finger homeobox 3 (ZFHX3) and transformation/transcription domain-associated protein (TRRAP) remained elevated after treatment, potentially promoting persistent inflammation via E2F transcription factor 1- (E2F1-) and E2F transcription factor 4- (E2F4-) mediated transcription. Among 1113 peptides identified by LC-MS/MS (selected using a significance threshold of < 0.05, without a fixed fold-change cutoff), 6-week treatment with BJK remedy significantly downregulated UBQLN1 (4.562-fold; = 0.016), suppressing toll-like receptor (TLR) activation and B-cell proliferation. It also upregulated Prostaglandin E synthase 2 (PTGES2) and PDZ and LIM domain protein 2 (PDLIM2) (7.841-fold and 8.697-fold, respectively; = 0.004 and 0.002), while enhancing antioxidant and immunoregulatory responses via ATP-binding cassette subfamily B member 8 (ABCB8) and ADP-ribosylation factor GTPase-activating protein 3 (ARFGAP3). By comparison, 3 weeks loratadine treatment significantly downregulated E2F transcription factor 3 (E2F3) and general transcription factor IIIC subunit 6 (GTF3C6) ( = 0.034 and 0.017) and upregulated CTD small phosphatase like 2 (CTDSPL2), suggesting a distinct but complementary anti-inflammatory mechanism. Together, these findings enhance the understanding of AR pathophysiology and may help to elucidate the mechanisms of BJK remedy and loratadine in treatment, supporting the further development of targeted therapies and biomarkers. - Source: PubMed
Publication date: 2026/08/18
Tiyao VilailakRoytrakul SittirukJaresitthikunchai JanthimaCharoenlappanit SawanyaPhaonakrop NarumonHoungiam KatanchaleeMukkasombut NichamonKuropakornpong PranpornMakchuchit SunitaChanvimalueng WaipojDavies Neal MItharat Arunporn - While PDZ-LIM domain-containing protein (PDLIM2) suppresses lung cancer, its clinical significance and therapeutic potential remain to be fully explored. - Source: PubMed
Publication date: 2026/08/08
Ashouri KaramSun FanKrause HarrisElliott AndrewLiu Stephen VMa Patrick CHalmos BalazsXiao GutianVanderwalde AriNieva Jorge JQu Zhaoxia - Lung cancer is a leading cause of cancer‑related mortality worldwide, which underscores the need to identify novel targets for improving early detection, therapeutic efficacy, and long‑term patient outcomes. PDZ and LIM domain protein 2 (PDLIM2) is a multifunctional adaptor protein that plays a role in cancer biology, particularly in lung cancer. Although PDLIM2 exerts divergent functions across various cancer types, substantial clinical, genetic, and experimental evidence consistently supports its role as a tumor suppressor in lung cancer. PDLIM2 expression is markedly downregulated in the majority of lung tumors representing various histological subtypes and disease stages, and its loss is strongly associated with poor prognosis. Mechanistically, it functions as an E3 ubiquitin ligase or ubiquitin ligase enhancer to promote the degradation of key transcription factors, including NF‑κB/RelA and STAT3, thereby restraining tumor‑associated inflammation, proliferation, survival, immune evasion, and metabolic reprogramming. PDLIM2 downregulation in lung cancer occurs through coordinated genetic and epigenetic mechanisms, including loss of heterozygosity at chromosome 8p21, promoter hypermethylation, histone deacetylation, and oxidative stress‑driven transcriptional repression. Functionally, the restoration of PDLIM2 suppresses lung tumor growth, enhances chemosensitivity, and promotes antitumor immunity, including response to immune checkpoint inhibitors. In addition, a protumoral mechanism of PDLIM2 downregulation involves mitochondrial dysfunction and accumulation of oncometabolites that lead to the activation of hypoxia inducible factor‑1α signaling. Overall, PDLIM2 is emerging as a biomarker and therapeutic target for lung cancer management. - Source: PubMed
Publication date: 2026/07/03
Chuang Tsung-HsienGuo Jeng-HungYang Jing-XingTseng Jen-ChihWang Hung-JungLai Chao-Yang - Breast cancer is a life-threatening malignancy with subtle early symptoms, necessitating novel biomarkers and mechanistic insights. The tight junction protein CLDN6 plays a tumor-suppressive role in breast cancer, yet its underlying molecular mechanisms remain incompletely understood. Herein, we demonstrate that CLDN6 suppresses breast cancer growth by inducing autophagic cell death through METTL14-mediated m6A modification of SOX4 mRNA. Mechanistically, CLDN6 sequesters PDLIM2 at the cell membrane, reducing nuclear PDLIM2-mediated RelA ubiquitination. Accumulated RelA transcriptionally upregulates METTL14, enhancing SOX4 mRNA m6A modification and degradation, which attenuates PI3K/Akt signaling and triggers autophagic cell death. Moreover, protein expression analysis in breast cancer tissues and bioinformatics analyses reveal an association between the CLDN6/METTL14/SOX4 axis and patient prognosis. These findings identify the CLDN6/METTL14/SOX4 axis as a promising prognostic signature and potential therapeutic target for breast cancer, highlighting the interplay among tight junction protein, epigenetic modification, and autophagic cell death as a conceptual basis for multi-targeted therapeutic strategies. - Source: PubMed
Publication date: 2026/05/01
Jin QiuLiang YingyingQu HuinanQi DaDong YuanSun MinghaoLiu YafangQuan Chengshi