CAIX _ CA9 Antibody (Antigen Affinity Purified)
- Known as:
- CAIX _ CA9 Antibody (Antigen Affinity Purified)
- Catalog number:
- 10107-RP02
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- CAIX _ CA9 Antibody (Antigen Affinity Purified)
Related genes to: CAIX _ CA9 Antibody (Antigen Affinity Purified)
- Gene:
- CA9 NIH gene
- Name:
- carbonic anhydrase 9
- Previous symbol:
- -
- Synonyms:
- MN, CAIX
- Chromosome:
- 9p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-29
- Date modifiied:
- 2016-03-18
Related products to: CAIX _ CA9 Antibody (Antigen Affinity Purified)
Related articles to: CAIX _ CA9 Antibody (Antigen Affinity Purified)
- Background and objectives Ocular surface squamous neoplasia (OSSN) encompasses a spectrum of tumours, including conjunctival squamous intraepithelial neoplasia (CSIN), carcinoma in situ (CIS), and invasive squamous cell carcinoma (iSCC). The roles of biomarkers such as epidermal growth factor receptor (EGFR), matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), hypoxia-inducible factor-1α (HIF-1α), and carbonic anhydrase IX (CAIX) in OSSN progression are incompletely understood. This study aimed to investigate their expression patterns in Asian Indian OSSN tumours. Methods This observational immunohistochemistry (IHC) study was conducted on 21 formalin-fixed, paraffin-embedded tissue specimens from patients with CSIN, CIS, or iSCC. OSSN tumours were categorised into Group A (CSIN and CIS) and Group B (iSCC). Immunohistochemical staining was used to assess the expression of EGFR, MMP-2, MMP-9, HIF-1α, and CAIX. Statistical analysis was performed to determine significant differences in biomarker expression between the groups. Results Significantly higher expression of EGFR (P=0.03), MMP-2 (P=0.02), and CAIX (P=0.03) was observed in Group B (iSCC) compared to Group A (CSIN and CIS). MMP-9 expression did not differ significantly between the groups (P=0.14). HIF-1α expression in tumour cells was also not significantly different (P=0.41). HIF-1α expression in inflammatory cells was significantly higher in Group B (iSCC) compared to Group A (P=0.038). Interpretation and conclusions This study suggests that EGFR, MMP-2, and CAIX may play a role in OSSN progression from CSIN/CIS to iSCC. Elevated HIF-1α expression in inflammatory cells highlights the potential involvement of inflammation in OSSN development. These biomarkers may serve as potential therapeutic targets and could also be integrated into diagnostic tools for OSSN. - Source: PubMed
Ramachandran Remya GirijaParameswaran SowmyaRajagopal RamaBiswas JyotirmayKrishnakumar Subramanian - Oxygen availability is frequently compromised in solid tumours, making intratumoural hypoxia a common feature of cancer. In prostate cancer (PCa), hypoxia is strongly associated with aggressive disease and poor prognosis. Hypoxia-inducible factor (HIF) is the master transcriptional regulator mediating hypoxia adaptation and is mainly controlled through proteasomal degradation of its α-subunit by the ubiquitin-proteasome system (UPS). However, the contribution of deubiquitinases (DUBs) to HIF signalling in PCa remains largely unexplored. Using a computational strategy based on CA9 expression as a surrogate of HIF activity, we identified Ubiquitin-Specific Protease 29 (USP29) as a key regulator associated with hypoxia and tumour progression and severity in PCa. Mechanistically, USP29 functions as a noncanonical positive regulator of HIF-α stability in a catalytic-dependent manner. USP29 interacts with HIF-1α, reduces its poly-ubiquitination and protects it from proteasomal degradation across multiple cancer cell lines. Additionally, USP29 stabilizes HIF-2α acting on the C-terminal region of HIF-α. These findings uncover a novel regulatory layer of HIF signalling and highlight USP29 as a potential therapeutic target in hypoxia-driven PCa progression. - Source: PubMed
Publication date: 2026/05/13
Schober Amelie SMoreno-Cugnon LeireMartínez-Pérez LauraErcilla AmaiaZabala-Letona AmaiaVicente-Barrueco AdriánFagoaga-Eugui MaiderGarcia-Longarte SaioaCalle-Ciborro BlancaPérez-Andrés EncarnaciónCarlevaris OnintzaPozo SaraMendizabal IsabelMayor UgoCarracedo ArkaitzSée ViolaineBerra Edurne - The levels of the microRNA-processing enzyme DICER and the hypoxia associated marker carbonic anhydrase 9 (CA9) critically influence tumor growth, aggressiveness, and response to therapy. However, their prognostic value in patients treated with definitive chemoradiotherapy (CRT) for anal squamous cell carcinoma (ASCC) remains elusive. - Source: PubMed
Publication date: 2026/04/29
Onay Melisde Valk Adalbert FWeigert AndreasKalinauskaite GodaTinhofer IngeborgGani CihanFokas EmmanouilRödel ClausMartin DanielPiiper AlbrechtRödel Franz - Clear cell renal cell carcinoma (ccRCC) can transition from indolent, low-grade lesions to high-grade, lethal disease through a layered cascade of genomic, epigenomic, metabolic, and immune remodeling. The initiating event in ∼90% of ccRCC is loss of chromosome 3p, enabling biallelic inactivation of VHL and frequent co-loss of chromatin regulators PBRM1, BAP1, and SETD2. The order and combination of genetic alterations shape distinct evolutionary trajectories in ccRCC. PBRM1 loss, observed in approximately 55% of cases, is linked to angiogenic, initially low-grade tumors that may later progress to higher-grade disease. In contrast, BAP1 loss (∼15%) drives early high-grade, inflammatory, immune-enriched phenotypes associated with aggressive behavior and worse prognosis. Progression is further shaped by structural and copy-number events including, chromothripsis coupling 3p loss with 5q gain, and recurrent 9p and 14q losses and 8q gain further promote cell-cycle dysregulation, genomic instability, and metastatic competence. Functionally, VHL loss stabilizes HIF-2α, driving VEGF signaling and Carbonic Anhydrase IX (CA9) expression and coupling pseudohypoxia to metabolic reprogramming and redox protection (glutathione/SLC7A11). Proteogenomic and metabolomic studies further highlight nutrient addiction with GLUT1/ASCT2 upregulation and a stress-resistant metabolic shield linked to grade and therapy resistance. Single-cell and spatial atlases place these programs in anatomic setting. They show that invasive fronts with high epithelial-mesenchymal transition (EMT) activity co-localize with myeloid and regulatory T-cell niches dominated by IL-1β, NF-κB, IL-10, STAT3, and TGF-β, along with exhausted CD8 T cells, thereby promoting immune escape and invasion. Integrating these layers yields mechanism-based biomarkers and therapeutic nodes for risk-adapted precision treatment. - Source: PubMed
Publication date: 2026/04/20
Jena Rajat SubhraMishra Akhilesh - Diabetic retinopathy (DR) represents one of the most common microvascular complications of diabetes, and proliferative diabetic retinopathy (PDR) is the most vision-threatening form. Carbonic anhydrase IX (CA9), a hypoxia-inducible enzyme, has been implicated in several pathological processes, but its involvement in DR has not been clarified. In this study, three single nucleotide polymorphisms (rs3829078, rs2071676, and rs1048638) were genotyped in diabetic patients with and without DR. Clinical characteristics were compared between groups, and expression analyses were conducted using public databases and ARPE-19 cells under hyperglycemic and hypoxic conditions. No significant association was observed between variants and DR susceptibility in the overall cohort. However, among patients aged ≤60 years, carriers of the rs1048638 C/A and C/A + A/A genotypes exhibited a significantly increased risk of PDR. Expression quantitative trait locus (eQTL) data from the GTEx database revealed higher CA9 mRNA expression in tissues harboring the rs1048638 A allele. Moreover, both transcriptomic data and experiments demonstrated upregulation of CA9 in ARPE-19 cells exposed to high glucose and hypoxia. These findings suggest that the rs1048638 polymorphism may modulate CA9 expression and contribute to PDR development in younger diabetic patients through hypoxia- and glucose-related mechanisms. Collectively, our findings suggest that CA9 may serve as a potential risk biomarker associated with the progression of DR, particularly in younger patients. - Source: PubMed
Publication date: 2026/03/30
Liang I-ChiaChien Hsiang-WenWang KaiLee Chia-YiChou Ying-ErhYang Shun-Fa