polyclonal CPX1 | coproporphyrinogen III oxidase, isoform 1
- Known as:
- pab CPX1 | coproporphyrinogen III oxidase, isoform 1
- Catalog number:
- as06123
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Agrisera
- Gene target:
- polyclonal CPX1 | coproporphyrinogen III oxidase isoform 1
Ask about this productRelated genes to: polyclonal CPX1 | coproporphyrinogen III oxidase, isoform 1
- Gene:
- CPXM1 NIH gene
- Name:
- carboxypeptidase X, M14 family member 1
- Previous symbol:
- CPXM
- Synonyms:
- CPX-1, CPX1
- Chromosome:
- 20p13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-17
- Date modifiied:
- 2016-07-20
Related products to: polyclonal CPX1 | coproporphyrinogen III oxidase, isoform 1
guanine nucleotide binding protein alpha inhibiting activity polypeptide 1 (GNAI1) polyclonal antibodykinase suppressor of ras (KSR) polyclonal antibody(Alpha)_ 1 _ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_1_ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Biotin Conjugates) Phospho-Slingshot 1 isoform 1 antibodies Immunogen: peptide Host: Rabbit(clone CAT72-Fan) MHC - N_A Polyclonal(Draxin) C1ORf187 Polyclonal anbtibody Host: Rabbit Affinity purifed(Draxin) C1ORf187 Polyclonal Antibody Host Species: Rabbit Immunogen: peptide Epitope Location:(Draxin) C1ORf187, Host species: Rabbit, Polyclonal antibody(D_Lys(nicotinoyl)1,b_(3_pyridyl)_Ala3,3,4_dichloro_D_Phe5,Asn6,D_Trp7,b_(3_pyridyl)_D_Ala9,Nle11)_Substance P Salt _ Binding _ Synonym Spantide III SumFormula C83H102Cl2N18O13(D_Lys(nicotinoyl)1,b_(3_pyridyl)_Ala3,3,4_dichloro_D_Phe5,Asn6,D_Trp7,b_(3_pyridyl)_D_Ala9,Nle11)_Substance P Salt _ Binding _ Synonym Spantide III SumFormula C83H102Cl2N18O13(FITC-conjugates) Phospho-Slingshot 1 isoform 1 antibodies Immunogen: peptide Host: Rabbit(I) LightCycler 1. 0; (Internal Control can't be used for this system) ; (II) LightCycler2. 0; (III) PE5700, MJ_Opticon etc. single color systems; (IV) ABI7000, ABI7300, ABI7500, ABI7900, ABI StepO Related articles to: polyclonal CPX1 | coproporphyrinogen III oxidase, isoform 1
- Systemic sclerosis (SSc) is a heterogeneous autoimmune disease characterized by a paucity of reliable biomarkers for accurate diagnosis and subtype stratification. The considerable clinical variability between diffuse and limited cutaneous subtypes underscores an urgent need for molecular tools that can dissect this heterogeneity and guide therapeutic strategies. - Source: PubMed
Publication date: 2026/08/19
Zhao XiangyueHu KejianCui YinzhiLi WenLi ZhiyaoFeng PuXie WenpingXiang XingchengXu WenChen JunzhangWangzha PingcuoLong XiaoWang JiucunChu Haiyan - Gastric cancer (GC) remains a leading cause of cancer-related mortality worldwide, with current treatment strategies largely limited to surgery, chemotherapy, and targeted therapy. Although the glycoprotein CPXM1 has been implicated in tumorigenesis, its functional role and underlying molecular mechanisms in GC remain unclear. In this study, we demonstrated that CPXM1 is significantly upregulated in GC tissues, and that elevated CPXM1 expression is associated with an unfavorable prognosis in GC patients. Both in vitro and in vivo functional assays revealed that CPXM1 significantly promotes GC cell proliferation, invasion, and metastasis. Mechanistically, CPXM1 was found to facilitate epithelial-mesenchymal transition (EMT), a critical process driving cancer progression. Furthermore, we identified the transcription factor RUNX1 as a direct upstream regulator of CPXM1, which binds to the CPXM1 promoter and transcriptionally activates its expression. Collectively, these findings delineate a previously unrecognized RUNX1/CPXM1/EMT axis that contributes to GC malignant progression, highlighting CPXM1 as a potential diagnostic biomarker and therapeutic target. - Source: PubMed
Publication date: 2026/07/31
Jia PingXu FengmingZhou TaoWang PingpingChen HuipingZhang JingYuan XiaochenXu HaoxunOuyang Yu - Keloids are fibroproliferative scars that extend beyond the original wound margins and may cause pain, pruritus, and substantial psychosocial distress. Earlobe keloids are common, clinically distinctive lesions with high recurrence rates; however, the molecular mechanisms underlying their development remain incompletely characterized. Existing transcriptomic studies have largely focused on extracellular matrix genes, with limited integration of metabolism-related pathways. - Source: PubMed
Publication date: 2026/07/07
Tafner DanielleNaccarato Andressa MarangoniIsoldi Felipe ContoliFelix Gabriel de Almeida ArrudaNogueira Beatriz Ribeirode Morais Rafael Leite TavaresPesquero João BoscoGragnani Alfredo - Mitochondrial abnormalities correlate closely with multiple cancers, but the role of genes associated with mitochondrial pathways in ovarian cancer (OC) remains unclear. This study aimed to identify OC prognosis-related mitochondrial pathway-associated genes at single-cell and transcriptome levels. Public datasets (GSE184880, GSE54388, GSE18520, TCGA-OV) were retrieved. Using GSE184880, potential cell subpopulations and their tumor-control differentially expressed genes (DEGs) were identified, then intersected with GSE54388 key module genes to yield candidate genes. Univariate Cox regression and LASSO analyses were performed to screen prognostic genes, based on which a prognostic risk model was constructed and validated. Functional and localization analyses of prognostic genes, regulatory network construction, immune infiltration analysis, drug prediction, and expression verification were conducted. Pseudotime, cell communication and expression analyses were implemented at single-cell level. To account for patient-level variation, mixed-effects models using the MAST method were applied. Targeted GSEA focusing on mitochondrial functional pathways was performed. Clinical correlation, independent prognostic analysis, and computational functional inference were conducted. Eight cell types were observed by cell clustering and annotation, among which endothelial cells, fibroblasts, NK cells, and tissue stem cells were observed as potential cell subpopulations. TK1, VWF, CPXM1, WIPF3, APOLD1, MGST2, and PPA1 were identified as prognostic genes, and risk models constructed based on them had good performance and universality. Mixed-effects model analysis confirmed that 1200 DEGs remained significant after adjusting for patient-level variation, supporting the robustness of single-cell findings. These prognostic genes were found to be robust predictors of patient survival with inconsistent expression patterns in vitro, and may play important roles in the differentiation and development of key cells. Targeted GSEA revealed that mitochondrial respiration (electron transport chain/oxidative phosphorylation) and mitophagy were significantly suppressed in the high-risk group, while mitochondrial fusion/fission and ROS pathways did not reach significance. PPA1 was highly expressed in various cell types in the GSE184880 dataset. In the GSE54388 dataset, CPXM1 and WIPF3 were substantially downregulated in the tumor group. However, other prognostic genes displayed the opposite expression pattern. Single-cell functional inference showed that TK1 and APOLD1 were highly expressed in G2/M phase, while MGST2, PPA1, VWF, CPXM1, and WIPF3 were enriched in G1 phase. VWF showed the strongest positive correlation with the PI3K-AKT pathway. Clinical validation confirmed the independent prognostic value of the signature in advanced-stage OC (FIGO III/IV). Seven mitochondrial pathway-associated prognostic genes were identified in OC, with inconsistent survival and in vitro expression patterns, providing novel references for exploring potential therapeutic targets. - Source: PubMed
Ruan YuxinLiu XiaLin XianhongLi YiyingYang YunlingLin Feifeng - Gastric cancer (GC) remains a leading cause of cancer-related mortality worldwide, and the prognosis of advanced GC remains poor. Systematic identification of robust biomarkers through multi-cohort integration and computational prioritization may facilitate the discovery of novel therapeutic targets. - Source: PubMed
Publication date: 2026/06/27
Li XinChen JiahanTian HongpenZhang Guangjun