IAP4 _ BIRC5 (1_99)
- Known as:
- IAP4 _ BIRC5 (1_99)
- Catalog number:
- AM00329PU-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- IAP4 _ BIRC5 (1_99)
Related genes to: IAP4 _ BIRC5 (1_99)
- Gene:
- ACBD5 NIH gene
- Name:
- acyl-CoA binding domain containing 5
- Previous symbol:
- -
- Synonyms:
- DKFZp434A2417, KIAA1996
- Chromosome:
- 10p12.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-11
- Date modifiied:
- 2014-11-19
- Gene:
- AK9 NIH gene
- Name:
- adenylate kinase 9
- Previous symbol:
- C6orf224, AKD2, C6orf199, AKD1
- Synonyms:
- FLJ42177, FLJ25791, dJ70A9.1, MGC26954
- Chromosome:
- 6q21
- Locus Type:
- gene with protein product
- Date approved:
- 2009-03-13
- Date modifiied:
- 2015-10-15
- Gene:
- ASAP3 NIH gene
- Name:
- ArfGAP with SH3 domain, ankyrin repeat and PH domain 3
- Previous symbol:
- DDEFL1
- Synonyms:
- FLJ20199, UPLC1, CENTB6
- Chromosome:
- 1p36.12
- Locus Type:
- gene with protein product
- Date approved:
- 2001-03-27
- Date modifiied:
- 2016-10-05
- Gene:
- BIRC5 NIH gene
- Name:
- baculoviral IAP repeat containing 5
- Previous symbol:
- API4
- Synonyms:
- EPR-1, survivin
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-10
- Date modifiied:
- 2016-10-04
- Gene:
- CCR9 NIH gene
- Name:
- C-C motif chemokine receptor 9
- Previous symbol:
- GPR28
- Synonyms:
- GPR-9-6, CDw199
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-17
- Date modifiied:
- 2016-03-14
Related products to: IAP4 _ BIRC5 (1_99)
Related articles to: IAP4 _ BIRC5 (1_99)
- BIRC5 (survivin), an inhibitor of apoptosis protein, is overexpressed in most tumors and is associated with drug resistance, proliferation, and metastasis, while being largely undetectable in normal differentiated tissues. This unique expression pattern makes BIRC5 an exceptionally selective therapeutic target, offering the potential to maximize anticancer efficacy while minimizing systemic toxicity to healthy tissues. However, few BIRC5-targeted agents have advanced to late-stage clinical trials. - Source: PubMed
Publication date: 2026/04/28
Chang Yung-ChiehHuang Wei-LunSu Wu-ChouLeung EuphemiaCheng Fong-YuCheung Chun Hei Antonio - : We previously pioneered a multigene mRNA test, qMIDS, validated through an international multicohort study with geographically and ethnically diverse oral squamous cell carcinoma (OSCC) patients from Europe and Asia. This study aimed to repurpose the qMIDS test for nasopharyngeal carcinoma (NPC). A molecular test independent of Epstein-Barr virus (EBV) status would be clinically useful for risk stratification in NPC patients with undetectable or low levels of EBV. : This study investigated a Chinese cohort of 62 participants (18 donated normal nasopharyngeal mucosa (NPM) and 44 donated NPC tissue samples). Messenger RNA levels of 16 genes in each sample were quantified using the qPCR method, and an algorithm computed a malignancy index for cancer risk stratification. : We identified a unique 10-gene panel (containing eight target genes, namely NEK2, INHBA, FOXM1, TOP2A, BIRC5, CXCL8, NR3C1, and IVL, relative to two reference genes, YAP1 and POLR2A, collectively named qMIDS) that demonstrated the best overall diagnostic performance in segregating NPM from NPC, with AUC = 0.909 and positive/negative predictive values of 91% PPV and 78% NPV, respectively. Furthermore, we demonstrated prognostic value of qMIDS in segregating NPM from NPC stage III + IV, with AUC = 0.936, 92% PPV, and 84% NPV. : Here, we present a simple qPCR-based 10-gene mRNA test, qMIDS, with potential clinical utilities for rapid (1 h) prognostic stratification of NPC. Further studies involving geographically and ethnically independent NPC cohorts would be needed to validate the clinical use of qMIDS in non-endemic NPC populations. - Source: PubMed
Publication date: 2026/04/09
Liang YingyingMo ZhiwenTeh Muy-Teck - Hepatocellular carcinoma (HCC) presents with poor treatment outcomes, creating an urgent need for novel biomarkers to improve diagnosis, prognosis, and precision medicine. While the MYB family of oncogenes is implicated in cancer, the role and regulatory mechanisms of its member, particularly MYB proto-oncogene like 2 (MYBL2), remain underexplored in HCC. Therefore, this study aimed to systematically validate the clinical significance of MYBL2, elucidate its functional role in tumor progression and drug sensitivity, and identify its upstream regulatory mechanisms using an integrative machine learning and experimental framework. - Source: PubMed
Publication date: 2026/04/22
Yang Ya-LingHuang Ying-HsienLin Hung-Yu - Inhibitors of apoptosis proteins (IAPs) are endogenous apoptosis regulators conserved in many species. We used bioinformatics approaches, identified six members of the IAP gene family (named PtIAP-01 to PtIAP-06) in the genome of Portunus trituberculatus. We phylogenetically classified these PtIAPs into four distinct subfamilies, namely BIRC5, BIRC6, BIRC7-A, and BIRC7-B. All identified PtIAPs contained the characteristic baculoviral IAP repeat (BIR) domain. In addition, some PtIAP members were found to possess additional functional domains, including RING finger or UBC. The expression levels of the PtIAPs were tissue-specific. PtIAP-01 was highly expressed in immune-related tissues (intestine and hepatopancreas), PtIAP-05 dominated in muscle, while PtIAP-02, -03, -04, and -06 showed preferential expression in the eyestalk. Following Vibrio parahaemolyticus injection, the expression levels of PtIAP-01, -02 and -05 were significantly upregulated, reaching 1.64-, 3.48-, and 4.18-fold of the control group, respectively, indicating their potential involvement in anti-pathogen immunity. Fluorescence in situ hybridization (FISH), RNA interference (RNAi) and terminal deoxynucleotidyl transferase nick-end-labeling (TUNEL) apoptosis assays validated their function. FISH confirmed that PtIAP-01, -02, and -05 were in both the nucleus and cytoplasm of hepatopancreatic cells. Their fluorescence signals got stronger after V. parahaemolyticus infection (PtIAP-05 strongest). RNAi and TUNEL demonstrated that knockdown of PtIAP-01, -02, and -05 significantly increased the mortality and apoptosis rates of P. trituberculatus after V. parahaemolyticus challenge, and significant upregulation of downstream apoptotic effector genes (PtCaspase-1, -3, -8). These findings offer new insights into the innate immune mechanisms of crustaceans and lay a foundation for breeding disease-resistant strains. - Source: PubMed
Publication date: 2026/04/28
Pan JiayiPan HangfengZhang BingjieZhou XianfaLv JianjianWang XuezhongSun DongfangGao Baoquan - Psoriasis is characterized by abnormal keratinocyte proliferation and BIRC5, also known as survivin, plays a critical role in the pathogenesis of psoriasis. However, the regulatory role of BIRC5 in psoriasis progression remains unclear. To elucidate the mechanisms by which BIRC5 regulates psoriasis, we used a mouse model of imiquimod (IMQ)-induced psoriasis characterized by psoriasis area and severity index (PASI) scores and epidermal hyperplasia. Immunohistochemistry and western blotting were performed to assess cell proliferation, autophagy, and apoptosis in vivo. The M5 (Oncostatin-M, IL-22, TNF-α, IL-1α, and IL-17 A) was used to treat HaCaT cells for the psoriatic cell model. M5-triggered HaCaT cells were used to investigate the function of BIRC5 in cell proliferation, apoptosis, and autophagy in vitro. The deletion of BIRC5 alleviated IMQ-induced psoriasis-like skin lesions, reduced the PASI scores, and decreased epidermal thickness. Inhibition of BIRC5 suppressed proliferation, facilitated apoptosis, and activated autophagy in these IMQ-induced mice. Consistent with the animal experiment results, M5 accelerated the proliferation of HaCaT cells, whereas inhibited the apoptosis and autophagy of HaCaT cells; however, BIRC5 knockdown partially reversed these effects. Additionally, silencing BIRC5 inhibited the phosphorylation of PI3K, AKT, and mTOR. Furthermore, 3-MA or SC79 treatment negated the autophagy- and apoptosis-enhancing effect of BIRC5 inhibition, as well as the inhibitory effect on HaCaT cell proliferation. Collectively, BIRC5 may accelerate keratinocyte proliferation and inhibit keratinocyte apoptosis through PI3K/AKT/mTOR-mediated autophagy. - Source: PubMed
Publication date: 2026/04/29
Xie CuilinWu HaixiaChen YongjunZou Ailing