CALR Recombinant Protein
- Known as:
- CALR Recombinant Protein
- Catalog number:
- XW-RP3028
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CALR Recombinant Protein
Related genes to: CALR Recombinant Protein
- 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 Recombinant Protein
Related articles to: CALR Recombinant Protein
- S-palmitoylation is a reversible post-translational modification that adds palmitic acid onto cysteine residues of proteins through the formation of a thioester bond. The reaction is catalyzed by protein acyl transferases (PATs) and reversed by acyl protein thioesterases (APTs), also known as S-depalmitoylases. Here, we optimized acyl resin-assisted capture (acyl-RAC) for identifying S-palmitoylated proteins in the model eukaryote Dictyostelium discoideum. Using this optimized protocol and western blotting, we revealed S-palmitoylated proteins in D. discoideum including calcium-dependent cell adhesion protein A (CadA), calreticulin (CalR), and glucose-regulated protein 78 (Grp78). Overall, this work establishes acyl-RAC as a tool for studying S-palmitoylation in D. discoideum and reveals a subset of S-palmitoylated proteins in this model organism that can be further studied. - Source: PubMed
Publication date: 2026/05/06
Owiar Samer AKim William DavidHuber Robert Joseph - Myelofibrosis (MF) is a chronic myeloproliferative neoplasm characterized by progressive cytopenias, splenomegaly, and constitutional symptoms. The hallmark of MF pathophysiology is constitutive activation of JAK/STAT signaling, which, in the majority of cases, is associated with an acquired mutation in one of three driver mutations, JAK2, CALR, or MPL. Our growing understanding of the molecular biology of MPNs has resulted in regulatory approval of four JAK inhibitors (JAKi), which have demonstrated efficacy in improving symptom burden and reducing spleen size. Despite clear benefits of JAKi therapy, including evidence of improved survival, these therapeutic interventions have not established an ability to modify disease in terms of resolution of bone marrow fibrosis or molecular remissions. Therefore, recent emphasis has been on the development of novel therapies with informed targets outside of the JAK/STAT signaling pathway. Moreover, combination approaches utilizing JAK and non-JAK targeting agents underscore the potential for disease modification along with deeper and more durable clinical responses. Emerging combination strategies and their clinical development will be reviewed here, including investigations that pair JAKi therapy with BCL-2 family inhibitors, BET inhibitors, restored p53 cell death signals, telomerase inhibitors, PIM1 kinase inhibitors, and mutant CALR targeted therapies. While several combination clinical trials suggest improved spleen and symptom responses and the possibility of disease modification, toxicity profiles and optimal sequencing remain areas of active investigation. - Source: PubMed
Publication date: 2026/04/08
Metzger MeganHertz CharlesMascarenhas John - The comparative proviral and antiviral mechanisms underlying host responses to Dengue virus (DENV-2) and Zika virus (ZIKV) in neural progenitor cells remain poorly understood. In this study, we first performed weighted gene co-expression network analysis (WGCNA) on RNA-seq data obtained from 30 hNPC samples infected with DENV-2 and ZIKV to compare the proviral and antiviral responses by identifying key virus-associated modules, hub genes, and enriched pathways. A total of 4,587 genes were grouped into 12 co-expression modules. The turquoise module (867 genes) showed a strong positive correlation with DENV-2 infection, whereas the green module (479 genes) showed a strong positive correlation with ZIKV infection (r = 0.92, adjusted p < 1 × 10 ⁻ ¹²). Hub genes, including CALR in the turquoise module and HMGCS1 in the green module, were found to be associated with viral replication. Functional enrichment analysis (GO, KEGG, and Reactome) revealed that both viruses modulated virus-specific and similar proviral and antiviral pathways. Among specific proviral pathways, DENV-2 infection was primarily enriched for TGF-β signaling, whereas ZIKV infection mainly engaged host translation regulation and nucleic acid-binding pathways. Similar proviral responses included endoplasmic reticulum (ER) stress and protein-folding mechanisms. Unique antiviral responses were also observed: DENV-2 triggered p53-mediated pathways, PI3K-Akt and Hippo signaling, NF-κB signaling, oxidative stress responses, and immunoglobulin class switching, whereas ZIKV infection enriched apoptotic and inflammatory pathways. Similar antiviral responses included autophagy, ubiquitin-mediated protein degradation, and Rho GTPase effector pathways. Insights from this network-based molecular study may inform the development of potential therapeutic strategies for neurological diseases associated with DENV-2 and ZIKV. - Source: PubMed
Publication date: 2026/04/30
Owaresat J KDey DipttaSiam Md Ahashan HabibAnam Md AshrafulSiddiki Amam Zonaed - Calreticulin (CALR) mutations in essential thrombocythemia (ET) are associated with younger age, higher platelet counts, and lower thrombosis rates. The present study analyzes the demographic, laboratory, and clinical features of the CALR mutation and its prognostic impact. - Source: PubMed
Publication date: 2026/02/22
Aydin Gökhan SamiAksoy ElifYönal Hindilerden İpekDağlar Aday AynurGültürk EmineNalçaci MelihaHindilerden Fehmi - Novel therapies for myelofibrosis (MF) are needed, particularly after JAK inhibitor failure. This open-label, phase 1/2 study evaluated bomedemstat, an irreversible inhibitor of lysine-specific demethylase 1 (LSD1), in participants with MF refractory or resistant to, inadequately controlled by, or intolerant of approved therapies. Eighty-nine participants initially received bomedemstat 0.25, 0.5, or 0.6 mg/kg orally once per day titrated to achieve a target platelet count of ≥50 to ≤75 ´ 109/L. Primary end points were safety and change in spleen volume. Hematologic response and change in symptom burden, bone marrow fibrosis score, and variant allele frequency (VAF) were exploratory. Eighty-seven participants (97%) experienced ≥1 any-cause adverse event (AE), most commonly thrombocytopenia (48%) and dysgeusia (36%); 62 participants (69%) experienced ≥1 grade 3-5 AE. Three participants (3%) experienced AEs that led to death; none were related to treatment. Of 35 participants with spleen volume data at week 24, 23 (66%) had a reduction in spleen volume; 9 (26%) had a reduction of ≥20%. Mean platelet and white blood cell counts normalized over 24 weeks; hemoglobin levels remained stable. Participants reported improvement in most symptoms, including fatigue. Of 35 participants with baseline and week 24 data, 8 (23%) had improved bone marrow fibrosis by ≥1 grade per central review, and 21 (60%) were stable. Of 36 participants with CALR, JAK2, or MPL mutations and data at week 24, 56% had a reduction in VAF. Bomedemstat has manageable safety and clinical activity in participants with MF in need of an alternative therapy. This trial was registered at www.cinicaltrials.gov as #NCT03136185. - Source: PubMed
Publication date: 2026/04/29
Gill HarinderYacoub AbdulraheemGerds Aaron TShortt JakeRossetti James MMead Adam JGöthert Joachim RKoschmieder SteffenEwing JoanneHalpern Anna BPalandri FrancescaPassamonti FrancescoMesa Ruben AMarchetti MoniaHarrison Claire NVannucchi Alessandro MWatts Justin MWood John CRoss David MPeppe JenniferNatsoulis GeorgesRienhoff Hugh Young