CD167b DDR2 Ig antibody Ab host: Rabbit
- Known as:
- CD167b DDR2 Ig (anti-) Antibody production species: Rabbit
- Catalog number:
- 'AP14440PU-N
- Product Quantity:
- 0.4 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CD167b DDR2 antibody host: Rabbit
Related genes to: CD167b DDR2 Ig antibody Ab host: Rabbit
- Gene:
- DDR2 NIH gene
- Name:
- discoidin domain receptor tyrosine kinase 2
- Previous symbol:
- TYRO10, NTRKR3
- Synonyms:
- TKT
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-17
- Date modifiied:
- 2016-10-05
- Gene:
- PPP1R18 NIH gene
- Name:
- protein phosphatase 1 regulatory subunit 18
- Previous symbol:
- KIAA1949
- Synonyms:
- phostensin
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-02
- Date modifiied:
- 2016-10-05
Related products to: CD167b DDR2 Ig antibody Ab host: Rabbit
Related articles to: CD167b DDR2 Ig antibody Ab host: Rabbit
- Distant metastasis, predominantly to the liver, remains the leading cause of death in colorectal cancer (CRC), yet biomarkers that capture metastatic competence remain limited. Ferroptosis is an iron-dependent, lipid peroxidation-driven form of regulated cell death that can restrain tumor progression, but whether primary CRC from patients with liver metastasis shows ferroptosis-resistance-related features remains incompletely understood. In a small exploratory set of T-stage-matched primary CRC tumors with or without liver metastasis, we quantified glutathione redox and lipid peroxidation-related readouts and assessed SLC7A11 and GPX4 expression. We integrated GSE62321 transcriptomic profiles with a FerrDb ferroptosis gene set, evaluated prognosis in TCGA-COAD/READ, and performed genetic knockdown, MDA assays, C11-BODIPY lipid ROS staining, ferrostatin-1 rescue assays, and Transwell assays in CRC cell models. Primary tumors from patients with liver metastasis showed a more reduced redox profile and increased expression of core ferroptosis-suppressive proteins, consistent with enhanced ferroptosis resistance potential but not direct evidence of lower in vivo ferroptotic cell death. Integrative discovery highlighted fatty acid binding protein 4 (FABP4), α-synuclein (SNCA), and discoidin domain receptor 2 (DDR2) as CRC-LM-associated ferroptosis-related candidates. High expression of each gene was associated with unfavorable disease-free survival. In CRC cell models, including the lymph-node-metastasis-derived SW620 line and additional validation lines, silencing FABP4, SNCA, or DDR2 increased bulk MDA and/or C11-BODIPY-detected lipid ROS, altered ferroptosis susceptibility, and suppressed migratory and/or invasive phenotypes. Ferrostatin-1 partially rescued knockdown-induced viability loss, lipid ROS accumulation, and migratory/invasive defects, supporting involvement of ferroptosis-associated lipid peroxidation while not excluding broader stress-response mechanisms. FABP4, SNCA, and DDR2 are CRC-LM-associated ferroptosis-related candidates that modulate lipid peroxidation, ferroptosis susceptibility, and migratory/invasive phenotypes in CRC cell models, warranting further validation in viability-controlled and liver metastasis-specific models. - Source: PubMed
Publication date: 2026/06/30
Ge ZhengGuo WeiLi JingxinWang YanqingWang Kexin - Owing to its involvement in extracellular matrix-glial cell interactions, discoidin domain receptor 2 (DDR2) has emerged as a promising pharmacological target in various human diseases, including cancers and neurodegenerative disorders. Two allosteric inhibitors, WRG-28 and DDR2-IN-1, selectively target DDR2. Their therapeutic efficacy is likely to depend on blood-brain barrier (BBB) penetration; however, a lack of analytical methods has so far left their pharmacokinetic properties and BBB permeability profiles largely unexplored. In this study, a liquid chromatography-tandem mass spectrometry method was developed and validated for the simultaneous quantification of WRG-28 and DDR2-IN-1 in plasma and brain tissue. The extraction procedure was simple and based on protein precipitation followed by lipid removal. This analytical method met the acceptance criteria of the European Medicines Agency guidelines. The calibration range was linear from 1 to 1000 ng/mL for both compounds. In addition, five prediction software tools were used to estimate pharmacokinetic parameters relevant to the BBB penetration of the two compounds. Finally, the method was applied in preclinical pharmacokinetic studies using elacridar, an efflux transporter inhibitor. - Source: PubMed
Publication date: 2026/06/24
Gueroue PaulBurban AudreySharanek AhmadBougueon GuillaumeBouchet StéphaneDucint DominiqueMolimard MathieuDjabarouti SarahGuyon Joris - Precise measurements of small molecule-protein interactions are critical for drug discovery. However, most biochemical profiling platforms measure binding using recombinant kinase domains or proteins in cell lysates, which can miss conformational regulation present in intact living cells. Here, we used flow cytometry-based fluorescent probe cellular binding assays (FPCBA) to demonstrate that the anticancer drug dasatinib binds native, untagged ABL1 kinase with 3-6-fold higher affinity than NanoLuc- or mVenus-tagged constructs in living cells. We further used this method for in-cell profiling of 25 native kinases, revealing conformational regulatory mechanisms, including SRC autoinhibition and membrane-dependent conformational states of DDR1, DDR2, and EPHA4 that are absent or attenuated in biochemical assays. For these studies, coumarin-dasatinib probes spanning a range of fluorophore acidity (p 4.1-7.3) were optimized for intracellular target engagement. To enhance sensitivity of detection, we found that uptake of acidic probes can be promoted by expression of the organic anion transporter OATP1B3. Quantitative flow cytometry with NIST-standardized beads established that intracellular concentrations of an intermediate-acidity 6FC-dasatinib probe approximated extracellular concentrations in HEK293T cells at equilibrium. Cellular values of dasatinib and imatinib for 25 kinases by FPCBA were broadly concordant with kinobead LC/MS measurements in cancer cell lysates but diverged substantially from recombinant KINOMEscan values, with divergences attributable to competition with ATP, autoinhibition, and membrane-dependent conformational states in living cells. FPCBA enables profiling of native protein-small molecule interactions in a physiologically relevant cellular context. - Source: PubMed
Publication date: 2026/06/23
Cool Lillian MPawar JogendraSonam SonamKumari SmitaZhao Serena LiHu XiaojunLin ZhihongWu MengHu ShuiyingPeterson Blake R - Orofacial clefting (OFC) is among the most common birth defects and can occur either as part of a syndrome or in isolation (nonsyndromic, ns). Cleft palate only (CPO) is an OFC subtype. Here, we searched for novel nsCPO risk genes carrying homozygous and compound-heterozygous variants, by analyzing exome data from six sibling pairs with nsCPO born to unaffected parents. After stringent quality control and filtering, we identified 6 homozygous variants and 32 compound-heterozygous variants in 5 and 16 candidate genes, respectively. We prioritized DDR2, a collagen-activated receptor-tyrosine-kinase influencing extracellular matrix composition, as our top candidate for functional follow-up, since variants in this gene can cause Warburg-Cinotti syndrome, the phenotypic spectrum of which includes palatal abnormalities. Knock-down and knock-out of DDR2-orthologs in zebrafish caused craniofacial abnormalities resembling CPO in humans. Zebrafish immunostaining indicated that DDR2-orthologs were expressed in mature head muscle cells, while murine single-cell RNA-Sequencing data detected Ddr2 expression only in head muscle progenitor cells; the latter finding was confirmed in human embryo sections stained for DDR2. DDR2-expressing head muscle progenitor cells may influence extracellular matrix composition through DDR2-mediated signaling, thereby affecting outgrowth, elevation, and fusion of the palatal shelves, a previously postulated mechanism involved in palatogenesis. Most established OFC genes (e.g. CDH1, CTNND1, IRF6, and GRHL3) act via mechanisms related to epithelial integrity and periderm differentiation, whereas our data provide evidence supporting DDR2 as a risk gene for nsOFC that functions by influencing extracellular matrix composition. - Source: PubMed
Capecki Julia AShkuro HelenaYilmaz ÖznurSchmitt LisaChannab KhadijaLindenberg Tobias TKruse TeresaAchterrath SarahCrespo BertaSiewert AnnaBakhshi MostafaPantel LeandraLudwig Kerstin UGeyer MatthiasMangold ElisabethOdermatt BenjaminIshorst Nina - Cardiac calcification is an age-associated pathological process that contributes to cardiac dysfunction, arrhythmia, and sudden cardiac death, yet its underlying mechanisms remain unclear. Cardiac fibroblasts (CFs) have emerged as key mediators of ectopic calcification through osteogenic differentiation. Proprotein convertase subtilisin/kexin type 9 (PCSK9), a key regulator of cholesterol metabolism, has been implicated in cardiovascular pathology beyond its canonical role, but its involvement in cardiac calcification is unknown. In this study, aged mice exhibited cardiac dysfunction, interstitial fibrosis, and myocardial calcium deposition, accompanied by upregulation of osteogenic markers, including Runx2, OCN, and Osx. PCSK9 expression was increased in aged hearts and enriched in DDR2-positive cells. In vitro, senescent CFs displayed enhanced osteogenic differentiation, characterized by increased calcium deposition, alkaline phosphatase activity, and elevated expression of osteogenic markers. Recombinant PCSK9 promoted osteogenic differentiation in young CFs, whereas genetic deletion of PCSK9 attenuated these effects in senescent CFs. Pharmacological experiments suggest that PCSK9-mediated osteogenic differentiation is associated with activation of the ATF4 pathway and upregulation of Runx2 expression. These findings support a role for the PCSK9-ATF4-Runx2 signaling axis in osteogenic differentiation of CFs, providing new insights into age‑related cardiac calcification and identifying this pathway as a hypothesis‑generating candidate for future investigation. - Source: PubMed
Publication date: 2026/06/19
Liu GangCai QiuyaYe LinPan BinbinYe ChenjiZhang ShuhongSun YongkunCui ChaochuLu ChengbiaoWang Xianwei