INPPL1 antibody
- Known as:
- INPPL1 (anti-)
- Catalog number:
- orb101734
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- INPPL1 antibody
Related genes to: INPPL1 antibody
- Gene:
- INPPL1 NIH gene
- Name:
- inositol polyphosphate phosphatase like 1
- Previous symbol:
- -
- Synonyms:
- SHIP2
- Chromosome:
- 11q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-12
- Date modifiied:
- 2016-10-07
Related products to: INPPL1 antibody
Related articles to: INPPL1 antibody
- Conditions resulting in elevated fibroblast growth factor 23 (FGF23) cause hypophosphatemic rickets and osteomalacia. The most common of these is X-linked hypophosphatemia. In this review we will broadly discuss the other less common and clinically distinct forms of renal hypophosphatemia, with a focus on the autosomal dominant and autosomal recessive types. - Source: PubMed
Publication date: 2026/07/07
Ferreira Carlos RImel Erik A - Moyamoya disease (MMD) is a progressive cerebrovascular disorder characterized by stenosis or occlusion of the terminal portions of the internal carotid arteries and their proximal branches, accompanied by the formation of abnormal collateral vessel networks. It represents a leading cause of ischemic and hemorrhagic stroke in both pediatric and adult populations. However, a comprehensive understanding of the molecular drivers underlying the hallmark vascular pathology of MMD remains elusive. Emerging evidence indicates that dysregulated lipid metabolism significantly contributes to MMD susceptibility and disease severity; nevertheless, its precise mechanistic roles in MMD pathogenesis have not been thoroughly investigated. - Source: PubMed
Publication date: 2026/06/09
Lu ZhenweiQiu XianshengZhou LiweiLi XiaodongLu HanwenWang ShuoChen JunfuBian LifeiLin JianbinZhao WenpengZhao WujieGao XinZhang JinsenChen SifangLi ZhangyuWang Zhanxiang - Despite the similarities, Crohn's disease (CD) and ulcerative colitis (UC), the two major subtypes of inflammatory bowel disease (IBD), exhibit distinctions. The increasing burden of IBD necessitates discovering novel diagnostic markers. Considering the importance of distinguishing between CD and UC in selecting therapeutic strategies in clinical settings, this investigation focused on identifying subtype-specific blood biomarkers. - Source: PubMed
Publication date: 2026/05/04
Mokaram Doust Delkhah Arman - Src homology 2 domain-containing inositol-5 phosphatase 2 (SHIP2) is a key player in regulating the signaling by phosphoinositides and is involved in the modulation of cellular functions such as proliferation, adhesion, migration, and survival. SHIP2 works by dephosphorylating PIP to modulate the PI3K/AKT pathway, which plays a role in different standard and pathological conditions. SHIP2 appears to play a dual part in cancer, serving as a tumor suppressor in some instances and a tumor promoter in others. It is also involved in neurodegenerative diseases, including Alzheimer's disease. To understand the molecular mechanism of SHIP2, we solved its cryogenic electron microscopy (cryoEM) structure. Unexpectedly, the SHIP2 pleckstrin homology-related domain was found to associate with its C2 and phosphatase domains. This arrangement enables the catalytic domain to interact with the substrate, especially at higher concentrations of PIP or PI(3,4)P. Furthermore, SHIP2 forms oligomers on the membrane. Our findings suggest a mechanism by which SHIP2 activity may be regulated through interactions with membrane lipids. This provides structural insights into how domain organization and membrane association regulate its function in various physiological contexts. - Source: PubMed
Gupta JyotiLe Coq JohanneLietha DanielIzard Tina - Esophageal squamous cell carcinoma (eSCC) is an aggressive malignancy with poor prognosis and limited therapeutic options. The phosphoinositide 3-kinase (PI3K)/AKT pathway is frequently activated in eSCC, but clinical use of PI3K or AKT inhibitors is restricted by toxicity and compensatory signaling. SHIP2, an inositol 5-phosphatase encoded by INPPL1, modulates this pathway by converting PI(3,4,5)P to PI(3,4)P, thereby regulating AKT activation. We previously identified INPPL1 amplification as recurrent in eSCC and demonstrated that SHIP2 inhibition suppresses tumor growth and synergizes with PLK1 inhibition. Here, we extend these findings and show that SHIP2-PLK1 synergy is not confined to eSCC but is also observed in multiple colorectal cancer cell lines, revealing a conserved vulnerability across tumor types. Mechanistic analyses demonstrate that this synergy depends on PI3K/AKT signaling, with SHIP2 inhibition producing stronger effects than direct PI3K blockade, suggesting additional regulatory functions beyond canonical PI3K control. Furthermore, SHIP2 inhibition enhances the cytotoxic activity of standard chemotherapies, including 5-fluorouracil and paclitaxel, in eSCC cells. Importantly, these effects occur at sub-cytotoxic drug concentrations, indicating potential therapeutic benefit with reduced toxicity. Collectively, our results identify SHIP2 as a central regulator of the PI3K/AKT axis in eSCC and colorectal cancer and highlight its value as a combinatorial target. SHIP2 inhibition represents a promising strategy to potentiate existing chemotherapies and targeted agents, opening new avenues for the treatment of refractory gastrointestinal cancers. - Source: PubMed
Publication date: 2025/11/04
Gillet NadiaBodart CyrilBeck Benjamin