Ask about this productRelated genes to: HHIPL1 Blocking Peptide
- Gene:
- HHIPL1 NIH gene
- Name:
- HHIP like 1
- Previous symbol:
- KIAA1822
- Synonyms:
- -
- Chromosome:
- 14q32
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-21
- Date modifiied:
- 2018-11-16
Related products to: HHIPL1 Blocking Peptide
Related articles to: HHIPL1 Blocking Peptide
- Heart failure with preserved ejection fraction is proposed to be caused by endothelial dysfunction in cardiac microvessels. Our goal was to identify molecular and cellular mechanisms underlying the development of cardiac microvessel disease and diastolic dysfunction in the setting of type 2 diabetes. - Source: PubMed
Publication date: 2023/11/30
Rouault PaulGuimbal SarahCornuault LaurianeBourguignon CéliaFoussard NinonAlzieu PhilippeChoveau FrankBenoist DavidChapouly CandiceGadeau Alain-PierreCouffinhal ThierryRenault Marie-Ange - Genome-wide association studies have identified chromosome 14q32 as a locus for coronary artery disease. The disease-associated variants fall in a hitherto uncharacterized gene called HHIPL1 (hedgehog interacting protein-like 1), which encodes a sequence homolog of an antagonist of hedgehog signaling. The function of HHIPL1 and its role in atherosclerosis are unknown. - Source: PubMed
Publication date: 2019/06/05
Aravani DimitraMorris Gavin EJones Peter DTattersall Helena KKaramanavi ElisavetKaiser Michael AKostogrys Renata BGhaderi Najafabadi MaryamAndrews Sarah LNath MintuYe ShuStringer Emma JSamani Nilesh JWebb Tom R - Several studies have reported the role of hedgehog interacting protein-like 1 (HHIPL-1) in different pathologies, including cardiovascular disease. The aim of the present study was to analyze the association of HHIPL-1 (rs2895811) polymorphism with myocardial infarction (MI), cardiometabolic parameters, and traditional cardiovascular risk factors in the Mexican population. The polymorphism was genotyped using a TaqMan assay in 1023 patients with MI and 1105 controls. A similar distribution of the polymorphism was observed between studied groups. However, in patients group, the C allele was associated with a decreased risk of developing hypertriglyceridemia (OR = 0.757, P = 0.030, OR = 0.685, P = 0.020, OR = 0.691, P = 0.030), metabolic syndrome (OR = 0.746, P = 0.030, OR = 0.647, P = 0.005, OR = 0.670, P = 0.015, OR = 0.637, P = 0.005), and insulin resistance (OR = 0.681, P = 0.045). The results suggest that HHIPL-1 rs2895811 polymorphism is associated with cardiometabolic parameters in Mexican patients with MI. - Source: PubMed
Publication date: 2018/04/12
Rodríguez-Pérez José ManuelPosadas-Sánchez RosalindaBlachman-Braun RubenVargas-Alarcón GilbertoPosadas-Romero CarlosRodríguez-Cortés Adrián AsaelLópez-Bautista FabiolaTovilla-Zárate Carlos AlfonsoRojas-Toledo Emma XochitlBorgonio-Cuadra Verónica MarusaPérez-Hernández Nonanzit - Gli1 is an important signaling molecular in Hedgehog signaling pathway. In our study, we explored the adjustment effect of Hedgehog-Gli1 signaling pathway on chicken male germ cells differentiation based on the transcriptome-wide analyses of chicken ESCs, primordial germ cells (PGCs) and spermatogonia stem cells (SSCs) that were associated with male germ cell differentiation. We screened out Hedgehog signaling pathway and identified 8 candidated differentially expressed genes (DEGs), Wnt3a, Wnt16, Wnt8a, HHIPL1, Gli1, BMP6, BMP7 and TTLL4. These DEGs expression change trend among blastoderm, genital ridge and testes, from which ESCs, PGCs and SSCs were isolated was the same as RNA-Seq data with quantitative RT-PCR evaluation. Based on retinoic acid (RA) induction of ESCs to SSCs in vitro, Gli1 overexpression has the ability to induce ESCs differentiation and SSCs-like cells formation and high expression of related reproductive genes, like Cvh, C-kit, Blamp1, Prmd14, Stra8, Dazl, integrin α6 and integrin β1 and so on in vitro. While RNAi knockdown of Gli1 can protect ESCs from differentiating into SSCs and correspondingly reduce the expression of the associated reproductive gene in vivo and vitro. Immunochemistry results showed that Gli1 overexpression could increase the expression of PGCs markers Cvh and C-kit and SSCs markers integrin α6 and integrin β1 in vivo, while Gli1 knockdown can have the opposite effect in vivo and in vitro. PAS stain and flow cytometry (FCM) evaluation results indicated the quantity of germ cells is decrease or increase with Gli1 knockdown or overexpression. Collectively, these results uncovered a novel function of Gli1 and demonstrated Hedgehog-Gli1 signaling pathway involved in chicken male germ cell differentiation, where it acts as a facilitator. - Source: PubMed
Publication date: 2017/02/10
Li DongCheng ShaozeZhang WenhuiWang ManSun ChanghuaZhang ChenWang YilinJin JingZhang YaniLi Bichun - A genetic component influences the development of atherosclerosis in the general population and also in rheumatoid arthritis (RA). However, genetic polymorphisms associated with atherosclerosis in the general population are not always involved in the development of cardiovascular disease (CVD) in RA. Accordingly, a study in North-American RA patients did not show the association reported in the general population of coronary artery disease with a series of relevant polymorphisms (TCF21, LPA, HHIPL1, RASD1-PEMT, MRPS6, CYP17A1-CNNM2-NT5C2, SMG6-SRR, PHACTR1, WDR12 and COL4A1-COL4A2). In the present study, we assessed the potential association of these polymorphisms with CVD in Southern European RA patients. We also assessed if polymorphisms implicated in the increased risk of subclinical atherosclerosis in non-rheumatic Caucasians (ZHX2, PINX1, SLC17A4, LRIG1 and LDLR) may influence the risk for CVD in RA. 2,609 Spanish patients were genotyped by TaqMan assays. Subclinical atherosclerosis was determined in 1,258 of them by carotid ultrasonography (assessment of carotid intima media thickness and presence/absence of carotid plaques). No statistically significant differences were found when each polymorphism was assessed according to the presence/absence of cardiovascular events and subclinical atherosclerosis, after adjustment for potential confounder factors. Our results do not show an association between these 15 polymorphisms and atherosclerosis in RA. - Source: PubMed
Publication date: 2017/01/06
López-Mejías RaquelCorrales AlfonsoVicente EstherRobustillo-Villarino MontserratGonzález-Juanatey CarlosLlorca JavierGenre FernandaRemuzgo-Martínez SaraDierssen-Sotos TrinidadMiranda-Filloy José AHuaranga Marco A RamírezPina TrinitarioBlanco RicardoAlegre-Sancho Juan JRaya EnriqueMijares VerónicaUbilla BegoñaFerraz-Amaro IvánGómez-Vaquero CarmenBalsa AlejandroLópez-Longo Francisco JCarreira PatriciaGonzález-Álvaro IsidoroOcejo-Vinyals J GonzaloRodríguez-Rodríguez LuisFernández-Gutiérrez BenjamínCastañeda SantosMartín JavierGonzález-Gay Miguel A