DKK-1 Fc, Human
- Known as:
- DKK-1 Fc, Human
- Catalog number:
- P723-50
- Product Quantity:
- 50 ug
- Category:
- -
- Supplier:
- 101 Bio.
- Gene target:
- DKK-1 Human
Related genes to: DKK-1 Fc, Human
- Gene:
- DKK1 NIH gene
- Name:
- dickkopf WNT signaling pathway inhibitor 1
- Previous symbol:
- -
- Synonyms:
- SK, DKK-1
- Chromosome:
- 10q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-01
- Date modifiied:
- 2018-06-28
Related products to: DKK-1 Fc, Human
Related articles to: DKK-1 Fc, Human
- Secreted modulators of the Wingless (WNT) pathways are associated with cardiometabolic dysregulation. Among these, Dickkopf-1 (DKK1) and secreted frizzled-related protein-3 (sFRP3) are abundantly expressed in placental tissue and secreted into the maternal circulation. We hypothesized their plasma levels would be dysregulated in women with gestational diabetes mellitus (GDM) and correlate with indices of metabolic health. - Source: PubMed
Publication date: 2026/08/14
Ueland ThorMichelsen Annika ElisabetQvigstad ElisabethRoland Marie Cecilie PaascheWesterberg Ane CecilieMichelsen Trond MelbyeAukrust PålBollerslev JensLekva Tove - Following the publication of the above paper, the authors contacted the Editorial Office to explain that they had incorrectly assembled certain of the data included in the western blots featured in Fig. 2D on p. 1033, and wished to issue a corrigendum. Upon performing an independent analysis of the data in this paper in the Editorial Office, however, it came to light that the data in question were strikingly similar to data which had already been submitted to the same journal () in a paper written by different authors at a different research institute. Upon asking the authors for an explanation concerning these data, the authors presented to the office a series of blots related to the same experiments, including the purported integral blots associated with the published data. However, owing to a number of remaining uncertainties concerning the blots provided resulting from an additional assessment of the raw underlying data made using the software analysis program, the Editor of has decided that this paper should be retracted from the Journal on account of a lack of confidence in the originally presented data. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 46: 1029‑1038, 2020; DOI: 10.3892/ijmm.2020.4672]. - Source: PubMed
Publication date: 2026/08/28
Liu JunWu MinfeiFeng GuangLi RuiWang YangJiao Jianhang - Semen quality is a critical determinant of reproductive efficiency in poultry, yet its molecular regulation remains poorly understood. - Source: PubMed
Publication date: 2026/08/12
Zhang LeiSun GuoboZhu RuiLi XiaomingZhang GanshengDuan Xiujun - Achondroplasia is the most common genetic skeletal dysplasia associated with disproportionate short stature and is primarily caused by gain-of-function variants in the fibroblast growth factor receptor 3 (FGFR3) gene. Constitutive FGFR3 activation disrupts growth plate homeostasis and endochondral ossification through complex alterations in chondrocyte proliferation, differentiation, hypertrophy, extracellular matrix organization, and intracellular signaling. The increasing understanding of these mechanisms has enabled the transition from exclusively supportive management toward disease-modifying and precision-based therapeutic strategies. This narrative review aimed to critically synthesize current evidence on the genetic basis, molecular pathogenesis, growth plate abnormalities, and current and emerging targeted therapies in achondroplasia. - Source: PubMed
Publication date: 2026/08/21
Șerban Rebecca CristianaMitut-Veliscu AndreeaDumitra AlexandraMarica LianaPopescu CristinaCostache AndreiTeona ȘerbanRiza Anca-LeliaDirnu RodicaVarut Renata-MariaStreață Ioana - ObjectiveTo compare zone-specific expression patterns of catabolic proteases and senescence-related genes across chondrocyte subpopulations in osteoarthritis (OA) cartilage.DesignSingle-cell RNA sequencing data from 72,616 chondrocytes (11 human cartilage samples; 6 normal, 5 OA; GSE220243) were analyzed. Following quality control and Harmony-based batch correction, cells were clustered into 27 subpopulations and assigned to superficial (SZ), middle (MZ), deep (DZ), or calcified (CZ) zones using zone-specific gene set module scores. Developmental origin scoring, catabolic gene expression ranking, senescence scoring, and signaling pathway analysis were performed across all clusters.ResultsUpon zonal assignment, the MZ constituted the largest compartment (73.6%), followed by the SZ (21.9%) and CZ (4.5%), with no cluster assigned a dominant DZ identity. MMP13 and ADAMTS5 showed their highest per-cell expression in SZ clusters, with MMP13 most prominent in a FibroC-COL1A2 superficial cluster (c10). SZ chondrocytes harbored a constitutively encoded fibroblastic identity transcriptionally resembling perichondrial and synovial fibroblast programs, independent of OA status, with concurrent deficiencies in Wnt inhibitor (FRZB, DKK1, WIF1) and FGF chondroprotective signaling relative to MZ. Senescence was observed in terminally differentiated clusters of both SZ and MZ, where a constitutively senescence-prone niche in SZ associated with mTOR and HIF1A signaling was mechanistically distinct from the senescence program observed in the MZ clusters.ConclusionsThese findings identify the developmentally distinct SZ as a candidate catabolic and senescent focus in OA cartilage and a potential contributor to matrix degradation and target for zone-stratified therapeutic intervention. - Source: PubMed
Publication date: 2026/08/26
Kim YoonheeJung GaeunHan Seungwoo