Ask about this productRelated genes to: CORIN Blocking Peptide
- Gene:
- CORIN NIH gene
- Name:
- corin, serine peptidase
- Previous symbol:
- -
- Synonyms:
- PRSC, CRN, ATC2, Lrp4, TMPRSS10
- Chromosome:
- 4p12
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-10
- Date modifiied:
- 2015-08-24
Related products to: CORIN Blocking Peptide
Related articles to: CORIN Blocking Peptide
- The impact of the spinopelvic relationship on hip instability and impingement after total hip arthroplasty (THA) has led to growing interest in functional acetabular component position. Various surgical techniques and technological advancements have been introduced to optimize acetabular component placement by accounting for individual spinopelvic mobility patterns. The purpose of this study was to evaluate the accuracy of acetabular component positioning with the use of a patient specific instrument (PSI). - Source: PubMed
Publication date: 2026/05/06
Arpey Nicholas COwens Jessell MMontgomery WilliamJohnson Roseann MJennings Jason MDennis Douglas A - All Poly (AP) tibial unicompartmental knee arthroplasty (UKA) seems to have advantages in comparison with metal-based (MB) UKA, such as greater polyethylene thickness, wear resistance, bone stock preservation and lower implant costs. The objective of this retrospective study was to evaluate the short-term clinical-functional and radiographic results, complications and survivorship of AP UKA performed consecutively with a minimum follow-up of 2 years. - Source: PubMed
Publication date: 2026/05/20
Gaggiotti StefanoGaggiotti GabrielLustig SebastienBatailler CecileMonllau Joan CarlesGaggiotti SantinoCombalia Andreu - LingGui QiHua-3 decoction (LGQH-3) is a clinical formulation for heart failure with preserved ejection fraction (HFpEF) associated with fluid retention. As a derivative of Zhenwu Decoction, it embodies to the ethnopharmacological principles of warming "yang", promoting "qi" transformation, and draining water to manage cardiorenal fluid dysregulation. However, its pharmacological underlying mechanisms remain unclear. - Source: PubMed
Publication date: 2026/05/16
Liang XiaoyuChen ZiyiLiu SiyuWei YueLi ZhixuanMou YunyingLiu DongxinLi YaoHao XiaopengHuang LuqiDong Guoju - CARD9 is a genetically validated target for autoimmune disease, with human expression quantitative trait loci (eQTLs) linking elevated CARD9 expression to increased disease risk and lower CARD9 expression to protection. Notably, a rare variant leading to a C-terminal truncation of CARD9 (CARD9Δ11) and subsequent loss of function confers protection against inflammatory bowel disease. Despite its therapeutic potential, CARD9 has long been considered "undruggable" as an adaptor protein with complex biology and limited chemical tools. Here, we leverage a protein homeostasis screening strategy to discover that inhibition of casein kinase 2 (CK2/CSNK2) results in the depletion of CARD9, a mechanism conserved across immortalized cell lines and primary cells. Mechanistic studies revealed that CK2 directly binds and phosphorylates CARD9 in its predicted disordered region. CK2 inhibitors prevent this protein-protein interaction, leading to CARD9 destabilization. Furthermore, the interaction between CK2 and CARD9Δ11 is significantly attenuated and resistant to CK2-mediated protein stabilization. Finally, we demonstrate therapeutic proof of concept in vivo using CK2 inhibition to deplete CARD9 in a murine peritonitis model. Our study expands the scope of cellular consequences elicited by kinase inhibition, offers an unconventional approach for engaging a therapeutically intractable target, and identifies a novel mechanism that could contribute to disease protection conferred by the CARD9Δ11 allele. - Source: PubMed
Publication date: 2026/05/16
Kelly Aya MMerselis Leidy CCauston BenjaminCalder Olivia KChao HosonPrack MargaretStine Laurel BAmako YukaWang TaoYesilkanal Ali ECondon Kendall JPierce Meekyum OWatterson Scott HGuernon JasonAnand AmitSelvam SabariyaDagde SayaliHolzinger EmilyPiasecki LaurenPemberton Travis AFu EmilyJoint McKennaSandt HaydenSingh Ashish KWang TaiCobb DeniseNi XiaochunDavies Geraint H MCorin Alan FRoy SophieWilson Stephen C - Dislocation remains a potential complication after total hip arthroplasty (THA), even with the anterior approach, which is generally associated with lower instability rates. Obturator dislocation, although well-documented in native hips following high-energy trauma, is extremely rare in the context of THA and has not been previously described in patients with preoperative spinopelvic assessment. We report two cases of obturator dislocation following direct anterior approach THA in young female patients without medical comorbidities. Both dislocations occurred during extreme hip flexion combined with abduction and external rotation. In one case, closed reduction attempts initially failed, requiring reduction on a traction table. Radiographic and 3D analyses revealed shared features, including significant medialization of the acetabular component (10 mm), low combined anteversion (16° and 24°), and lumbopelvic mobility patterns dominated by hip flexion. Preoperative functional imaging showed no signs of spinopelvic imbalance or stiffness. Both patients exhibited a "hip user" profile with low pelvic incidence and distal lumbar lordosis apex. These cases highlight multiple converging factors contributing to instability: loss of offset due to cup medialization, stem retroversion resulting in low combined anteversion, and postoperative increase in compensatory hip flexion. Notably, no classic spinopelvic risk factors were present. These findings underscore the need for precise implant positioning, especially for acetabular positioning and femoral version. - Source: PubMed
Publication date: 2026/05/10
Peynet BriacAim FlorenceAuberger GuillaumeBouy AloisAubert Thomas