Ask about this productRelated genes to: INPP5D Blocking Peptide
- Gene:
- INPP5D NIH gene
- Name:
- inositol polyphosphate-5-phosphatase D
- Previous symbol:
- -
- Synonyms:
- SHIP, hp51CN, SHIP1
- Chromosome:
- 2q37.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-04-04
- Date modifiied:
- 2015-08-13
Related products to: INPP5D Blocking Peptide
Related articles to: INPP5D Blocking Peptide
- The GID/CTLH E3 ligase complex is implicated in several biological processes, yet its full substrate repertoire remains poorly defined. We recently identified the complex as a broad modulator of macrophage responses to (Mtb) infection. Here, we use label-free proteomics and diGly capture analysis of Mtb-infected macrophages to define the GID/CTLH-dependent ubiquitylome. We identify thousands of dynamically altered ubiquitylation sites, with strong enrichment among proteins involved in cellular metabolism and innate immune signaling. Concurrent proteome analysis revealed extensive rewiring in GID/CTLH-deficient macrophages, with >90% of enriched pathways among increased proteins consisting of metabolic targets. Notably, inhibitory phosphatases (PTEN, INPP5D) also emerged as candidate substrates. Functional studies revealed proteasome-dependent stabilization of PTEN and INPP5D in GID/CTLH-deficient macrophages with each phosphatase individually exerting an influence on Mtb intracellular survival. Together, our study defines a GID/CTLH-dependent ubiquitylome in macrophages and identifies the complex as a central regulator of metabolism and antimicrobial immunity. - Source: PubMed
Publication date: 2026/04/27
Simwela Nelson VJohnston LuanaSassetti Christopher MRussell David G - Cognitive impairment (CI) is a prevalent and debilitating non-motor symptom in Parkinson's disease (PD), yet reliable early diagnostic biomarkers are lacking. This study aimed to identify serum biomarkers associated with PD-CI and investigate the synergistic contributions of lipid metabolism and inflammatory signaling. - Source: PubMed
Publication date: 2026/04/15
Su MingyuYang TianshuFan XinruiQiang XiyuLiao ZihanGu HengGao LinyunChen RuiTang ChuanxiMu Chunyan - - Source: PubMed
Publication date: 2026/04/22
Xi RongjiaoZheng XiaoboZhao JingFu Yuan - Autophagy-mitophagy pathways are essential for regulating immune homeostasis. However, their contribution to population-level chronic low-grade systemic inflammation (SI) remains unclear. The objective was to investigate the association between variation in the genes related to the autophagy-mitophagy pathways and SI, and to examine whether lifestyle factors modify this relationship. We conducted genome-wide association studies and gene-set enrichment analyses using data from the Korean Genome and Epidemiology Study (KoGES, n = 28,102) and UK Biobank (UKBB, n = 343,892). SI was defined as an elevated white blood cell count or high-sensitivity C-reactive protein. Using Core Longevity State Vectors (CLSVs)-gene sets representing immune-longevity pathways derived from comparative transcriptomic analysis-we tested six pathways and constructed a weighted genetic risk score (GRS) from significant variants. Gene-lifestyle interactions were examined with respect to major dietary and lifestyle factors. Among six CLSVs, only CLSV-2 (mitophagy and autophagy) showed a significant association with SI (β = 0.425, = 0.008). Six single nucleotide polymorphisms (SNPs) in autophagy-mitophagy genes (, , , , , and ) were associated with SI in KoGES ( < 5 × 10), and ten SNPs (genes selected in KoGES plus , , , ) reached genome-wide significance in UKBB ( < 5 × 10). A higher GRS was associated with increased SI in both cohorts and was strongly associated with metabolic syndrome (MetS, OR = 1.91 in KoGES; OR = 1.62 in UKBB). SI was characterized by neutrophilia with relative lymphopenia. In UKBB, significant gene-lifestyle interactions were observed for diet, physical activity, smoking, and alcohol ( < 0.01). Favorable lifestyle factors reduced SI most effectively in individuals with protective genotypes. Among individuals with a high vegetable/fruit intake, SI prevalence was 35%, 36%, and 38% in the negative-, zero-, and positive-GRS groups, respectively, compared with 36%, 45%, and 48% in the low-intake groups. In conclusion, genetic variations in autophagy-mitophagy pathways specifically influence SI. Genetic predisposition substantially modifies the benefits of lifestyle, underscoring the importance of integrating genetic and lifestyle factors in understanding SI susceptibility. - Source: PubMed
Publication date: 2026/03/27
Choi YoungjinPark Sunmin - FCRL1 is a plasma membrane coreceptor on B cells that has been shown to potentiate B cell receptor (BCR)-driven calcium flux and negatively regulate ERK phosphorylation in a GRB2 and tyrosine-dependent manner. Of the proteins that associate with FCRL1, the recruitment of the inositol phosphatase SHIP-1 is GRB2 dependent, implicating SHIP-1 in FCRL1-mediated ERK regulation. Using immunoprecipitation and Western blotting, it was found that a proline-rich region in the C-terminus of SHIP-1, rather than its N-terminal SH2 domain, mediates recruitment of SHIP-1 to Y281 in FCRL1 in a manner dependent on GRB2. Interestingly, Y281 and GRB2 were also required for FCRL1 colocalization to the BCR. Translational fusions between tyrosine-mutated FCRL1 and the SH2 domain of SHIP-1 were sufficient to drive both colocalization of FCRL1 with the BCR as well as the ERK-inhibitory activity of FCRL1. Our data are consistent with a function for SHIP-1 as an adapter between FCRL1 and the BCR signalosome, and that this adapter function is responsible for BCR/FCRL1 colocalization after BCR stimulation and modulation of ERK signaling. - Source: PubMed
Wolfe Malory MTallon Arranz RutZenni Elizabeth LWilson Timothy J