CALR & APP Protein Protein Interaction Antibody Pair
- Known as:
- CALR & APP Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0055
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- CALR & APP Protein Interaction Antibody Pair
Ask about this productRelated genes to: CALR & APP Protein Protein Interaction Antibody Pair
- Gene:
- CALR NIH gene
- Name:
- calreticulin
- Previous symbol:
- -
- Synonyms:
- RO, SSA, cC1qR, CRT, FLJ26680
- Chromosome:
- 19p13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2019-04-23
Related products to: CALR & APP Protein Protein Interaction Antibody Pair
Related articles to: CALR & APP Protein Protein Interaction Antibody Pair
- Myeloproliferative neoplasms (MPN) are rare hematological malignancies with long survival, making real-world evidence essential to complement clinical trial data. The Danish National Chronic Myeloid Neoplasia Registry (DMR) captures nearly all MPN patients nationwide, but its validity has not been systematically evaluated. We aimed to validate key clinical variables in the DMR through a nationwide audit. - Source: PubMed
Publication date: 2026/04/15
Patel Dustin AndersenKannik KarinaChanchiri ImanBrown Peter de NullyRoug Anne StidsholtGrønbæk KirstenBak MarieEl-Galaly Tarec ChristofferAndersen Christen Lykkegaard - - Source: PubMed
Publication date: 2026/04/07
Ginley KatelynSolanki ShipraConnington Rachael AChallagundla Kishore BSolanki Ranjan - Essential thrombocythemia (ET) is a myeloproliferative neoplasm characterized by elevated platelet counts and risks of both thrombosis and bleeding. Acquired von Willebrand disease is a rare complication of ET, particularly in extreme thrombocytosis. We report a 32-year-old man diagnosed with ET, acquired von Willebrand disease, and autoimmune gastritis with vitamin B12 deficiency. He presented with marked thrombocytosis (1,340 × 10/L), reduced von Willebrand factor activity, low vitamin B12 levels, and positive parietal cell antibodies, but remained asymptomatic. The coexistence of these 3 conditions is rarely reported and may represent a form of beneficial autoimmunity, in which autoimmune phenomena paradoxically confer protective effects against thrombotic complications. - Source: PubMed
Publication date: 2026/04/17
Marfo EmmanuelAjayi AbisolaBass Kyla JCrawford Marvin LLuévano Jesús M - Environmental pollutant exposure has been associated with chronic kidney disease (CKD), yet specific chemicals related to renal function variation remain incompletely characterized. - Source: PubMed
Publication date: 2026/04/13
Zhou XiaoshanDeng WeitianChu ChengshuangWu QingqingCao YuqingChen WanjiaLiu WangyiYue LingXiao ShifuLi QingrunYin YuanyuanGao XiaojingZeng RongDeng Yueyi - This review highlights the emergence of CALR as a promising therapeutic target in CALR-mutated myeloproliferative neoplasms. While current JAK inhibitors alleviate symptoms and reduce thrombosis risk, they lack clonal specificity, have a limited impact on the natural history of disease, and are limited by toxicity and resistance. In contrast, CALR mutations generate a unique, disease-specific neoepitope that drives disease pathogenesis through aberrant MPL activation and is accessible on the cell surface, making it an ideal immunologic and antibody target. Preclinical and early clinical advances - including monoclonal antibodies, bispecific T-cell engagers, CAR-T therapies, antibody-drug conjugates, and peptide/viral vector vaccines - have demonstrated selective activity against CALR-mutant clones while sparing normal hematopoiesis, with encouraging evidence of molecular remissions and disease modification. Although challenges such as immune tolerance remain, mutant CALR-directed therapies represent a potential transformative shift in essential thrombocythemia, and primary myelofibrosis treatment. - Source: PubMed
Publication date: 2026/04/19
Soni AnushriVerma AmitGoel Swati