Human Persephin (PSP) Source E. coli
- Known as:
- Human Persephin (PSP) Source E. coli
- Catalog number:
- 100-120
- Product Quantity:
- 20 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Human Persephin (PSP) Source . coli
Related genes to: Human Persephin (PSP) Source E. coli
- Gene:
- BPIFA2 NIH gene
- Name:
- BPI fold containing family A member 2
- Previous symbol:
- C20orf70
- Synonyms:
- bA49G10.1, SPLUNC2, PSP
- Chromosome:
- 20q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 2001-07-17
- Date modifiied:
- 2015-12-07
- Gene:
- FCN2 NIH gene
- Name:
- ficolin 2
- Previous symbol:
- -
- Synonyms:
- P35, FCNL, EBP-37, ficolin-2
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-07-11
- Date modifiied:
- 2016-10-05
- Gene:
- FDPSP6 NIH gene
- Name:
- farnesyl diphosphate synthase pseudogene 6
- Previous symbol:
- FDPSP
- Synonyms:
- -
- Chromosome:
- 21q21.1
- Locus Type:
- pseudogene
- Date approved:
- 2000-05-23
- Date modifiied:
- 2014-11-19
- Gene:
- GPR45 NIH gene
- Name:
- G protein-coupled receptor 45
- Previous symbol:
- -
- Synonyms:
- PSP24, PSP24A
- Chromosome:
- 2q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-03-12
- Date modifiied:
- 2016-10-05
- Gene:
- GPR63 NIH gene
- Name:
- G protein-coupled receptor 63
- Previous symbol:
- -
- Synonyms:
- PSP24(beta), PSP24B
- Chromosome:
- 6q16.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-05
- Date modifiied:
- 2016-10-06
Related products to: Human Persephin (PSP) Source E. coli
Related articles to: Human Persephin (PSP) Source E. coli
- Myocardial injury activates the complement lectin pathway (LP) in acute coronary syndrome (ACS) and LP inhibition improved cardiac function in experimental studies, suggesting a direct pathogenic role. The clinical consequences of LP activation are insufficiently defined. We investigated how plasma levels of the LP activators mannose-binding lectin (MBL) and ficolin-2 (FCN2) relate to cardiac recovery and prognosis in ACS patients. - Source: PubMed
Publication date: 2026/07/24
Zhong BaojunKing BenMares Razvan GheorghitaArbanasi Emil-MarianYndigegn TroelsEngelbertsen DanielBjörkbacka HarryNilsson JanGoncalves IsabelBlom AnnaSchiopu Alexandru - The first wave of Coronavirus disease 2019 (COVID-19), driven by the global emergence of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), severely affected Spain with high infection and mortality rates across the country. Although numerous common and rare genetic variants affecting immune-related pathways have been associated with susceptibility to infection and severe disease, the contribution of complement system remains comparatively understudied. - Source: PubMed
Publication date: 2026/06/11
De La Morena-Barrio María EugeniaVan Den Rym AnaEscorial Sanz OlgaCorvillo FernandoGarcía-Sánchez RosarioGonzález-Sánchez LauraMuñoz-Barrera AdriánGonzález-Montelongo RafaelaLorenzo-Salazar José MiguelFlores Carlosde Andrés-Martín AnaRodríguez-Gallego CarlosAllende LuisAlsina LaiaSánchez-Ramón SilviaLópez-Collazo EduardoLópez-Trascasa MargaritaSánchez-Corral PilarPérez de Diego RebecaCorral de la Calle JavierLópez-Lera Alberto - The complement system has an important role in physiological bone healing, as studied mainly in animal models and local bone tissues. However, the role of the complement system in human fractures, particularly at the systemic level, remains insufficiently characterized. This study aimed to investigate the activation levels of the serum complement system during three healing phases (inflammation, repair and remodeling) of normal healing of long bone fractures and in patients diagnosed with fracture non-union. - Source: PubMed
Publication date: 2026/06/09
El-Sherbiny Yasser MAli Youssif MJones ElenaGiannoudis Peter VEl-Jawhari Jehan J - Down syndrome (DS), or trisomy 21 (T21), resulting from an extra copy of chromosome 21, occurs in 1 in 700-1,000 live births. Neuroinflammation is increasingly recognized as a critical contributor to DS neuropathology, although its underlying drivers remain unclear. - Source: PubMed
Publication date: 2025/12/05
Teles E Silva André LuízPrado de Oliveira Pedro HenriqueYokota-Moreno Bruno Yukioda Silva Fausto JéssicaAvila Jonatan PeñaNakaya Helder ISertié Andréa LauratoZampieri Bruna Lancia - Ficolins, encoded by FCN genes, are key pattern recognition molecules of the lectin complement pathway involved in immune complex clearance, a process often impaired in systemic lupus erythematosus (SLE). Genetic polymorphisms in FCN genes may influence disease susceptibility. However, their functional significance in SLE remains unclear. The present study aimed to investigate the association of selected FCN gene single-nucleotide polymorphisms (SNPs) with SLE, lupus nephritis (LN), and serum ficolin levels in a Western Indian cohort. Seven SNPs in FCN1 (rs2989727, rs1071583), FCN2 (rs7851696, rs17549193, rs7865453, rs17514136), and FCN3 (rs3813800) were genotyped in 200 SLE patients and 200 healthy controls using polymerase chain reaction (PCR) sequence-specific primer and PCR restriction fragment length polymorphism. Serum ficolin-1, -2, and -3 levels were measured using ELISA. Statistical analysis included χ2 test, Kruskal-Wallis test, and logistic regression to assess associations and calculate odds ratios with 95% confidence intervals. The analysis identified significant associations of FCN2 rs7851696, rs7865453, and rs17514136, as well as FCN3 rs3813800, with SLE susceptibility. Among LN patients, FCN1 rs2989727 and rs1071583, FCN2 rs17514136, and FCN3 rs3813800 showed significant associations. FCN3 rs3813800 was significantly associated with ficolin-3 levels, while FCN2 rs7865453 was associated with complement component 1q-circulation immune complex levels. These findings provide novel insight into associations of FCN gene polymorphisms with SLE and LN susceptibility, with genotype-phenotype correlations suggesting their biological relevance. Future longitudinal and mechanistic studies are warranted to validate these associations and explore their therapeutic potential. - Source: PubMed
Rai KirtiKhatri RidiJose AmruthaNadkar MilindRajadhyaksha AnjaliKonkar HarshadaSamant TrishaJaiswal PoojaDabholkar KunalPawaskar SwapnalMalik AmanParande AltafBitla GauthamiTapase PrashantPadwal VijayMadkaikar ManishaPradhan Vandana D