Ask about this productRelated genes to: SSFA2 antibody
- Gene:
- ITPRID2 NIH gene
- Name:
- ITPR interacting domain containing 2
- Previous symbol:
- SSFA2
- Synonyms:
- CS-1, SPAG13, KRAP, KIAA1927
- Chromosome:
- 2q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-16
- Date modifiied:
- 2018-06-15
Related products to: SSFA2 antibody
Related articles to: SSFA2 antibody
- Bladder cancer (BLCA) has a poor prognosis and continues to pose a significant challenge for clinicians. Prior studies have demonstrated a close relationship of BLCA with macrophages. However, the key subpopulations and molecular functions of macrophages in BLCA have not been uncovered. It becomes possible to use single-cell sequencing technology to explore macrophage heterogeneity and identify new biomarkers. - Source: PubMed
Publication date: 2025/10/04
Che GuangliangZhao XuejunLuo RongtuanYu QuanfengGuo XiaofengGao KeChen KangyuZhang Erfeng - The correlation between hypoxia and tumor development is widely acknowledged. Meanwhile, the foremost organelle affected by hypoxia is mitochondria. This study aims to determine whether they possess prognostic characteristics in lung adenocarcinoma (LUAD). For this purpose, a bioinformatics analysis was conducted to assess hypoxia and mitochondrial scores related genes, resulting in the successful establishment of a prognostic model. Using the single sample Gene Set Enrichment Analysis algorithm, the hypoxia and mitochondrial scores were computed. Differential expression analysis and weighted correlation network analysis were employed to identify genes associated with hypoxia and mitochondrial scores. Prognosis-related genes were obtained through univariate Cox regression, followed by the establishment of a prognostic model using least absolute shrinkage and selection operator Cox regression. Two independent validation datasets were utilized to verify the accuracy of the prognostic model using receiver operating characteristic and calibration curves. Additionally, a nomogram was employed to illustrate the clinical significance of this study. 318 differentially expressed genes associated with hypoxia and mitochondrial scores were identified for the construction of a prognostic model. The prognostic model based on 16 genes, including PKM, S100A16, RRAS, TUBA4A, PKP3, KCTD12, LPGAT1, ITPRID2, MZT2A, LIFR, PTPRM, LATS2, PDIK1L, GORAB, PCDH7, and CPED1, demonstrates good predictive accuracy for LUAD prognosis. Furthermore, tumor microenvironments analysis and drug sensitivity analysis indicate an association between risk scores and certain immune cells, and a higher risk scores suggesting improved chemotherapy efficacy. The research established a prognostic model consisting of 16 genes, and a nomogram was developed to accurately predict the prognosis of LUAD patients. These findings may contribute to guiding clinical decision-making and treatment selection for patients with LUAD, ultimately leading to improved treatment outcomes. - Source: PubMed
Publication date: 2024/06/17
Zhao WenhaoHuang HuaZhao ZexiaDing ChenJia ChaoyiWang YingjieWang GuannanLi YongwenLiu HongyuChen Jun - Inositol 1,4,5-trisphosphate (IP3) receptors (IP3Rs) are high-conductance channels that allow the regulated redistribution of Ca2+ from the endoplasmic reticulum (ER) to the cytosol and, at specialized membrane contact sites (MCSs), to other organelles. Only a subset of IP3Rs release Ca2+ to the cytosol in response to IP3. These 'licensed' IP3Rs are associated with Kras-induced actin-interacting protein (KRAP, also known as ITPRID2) beneath the plasma membrane. It is unclear whether KRAP regulates IP3Rs at MCSs. We show, using simultaneous measurements of Ca2+ concentration in the cytosol and mitochondrial matrix, that KRAP also licenses IP3Rs to release Ca2+ to mitochondria. Loss of KRAP abolishes cytosolic and mitochondrial Ca2+ signals evoked by stimulation of IP3Rs via endogenous receptors. KRAP is located at ER-mitochondrial membrane contact sites (ERMCSs) populated by IP3R clusters. Using a proximity ligation assay between IP3R and voltage-dependent anion channel 1 (VDAC1), we show that loss of KRAP reduces the number of ERMCSs. We conclude that KRAP regulates Ca2+ transfer from IP3Rs to mitochondria by both licensing IP3R activity and stabilizing ERMCSs. - Source: PubMed
Publication date: 2024/06/27
Atakpa-Adaji PeaceIvanova AdelinaKujawa KarolinaTaylor Colin W - Head and neck cancer (HNC) is the sixth most common malignancy worldwide. Although current modalities offer a wide variety of therapy choices, head and neck carcinoma has poor prognosis due to its diagnosis at later stages and development of resistance to current therapeutic tools. In the current study, we aimed at exploring the roles of miR-200c-3p during head and neck carcinogenesis and acquisition of taxol resistance. We analyzed miR-200c-3p levels in HNC clinical samples and cell lines using quantitative real-time polymerase chain reaction and evaluated the effects of differential miR-200c-3p expression on cancer-related cellular phenotypes using in-vitro tools. We identified and characterized a direct target of miR-200c-3p using in-silico tools, luciferase and various in-vitro assays. We investigated potential involvement of miR-200c-3p/SSFA2 axis in taxol resistance in-vitro. We found miR-200c-3p expression as significantly downregulated in both HNC tissues and cells compared to corresponding controls. Ectopic miR-200c-3p expression in HNC cells significantly inhibited cancer-related phenotypes such as viability, clonogenicity, migration, and invasion. We, then, identified SSFA2 as a direct target of miR-200c-3p and demonstrated that overexpression of SSFA2 induced malignant phenotypes in HNC cells. Furthermore, we found reduced miR-200c-3p expression in parallel with overexpression of SSFA2 in taxol resistant HNC cells compared to parental sensitive cells. Both involved in intracellular cytoskeleton remodeling, we found that SSFA2 works collaboratively with IP3R1 to modulate resistance to taxol in HNC cells. When considered collectively, our results showed that miR-200c-3p acts as a tumor suppressor microRNA and targets SSFA2/IP3R1 axis to sensitize HNC cells to taxol. - Source: PubMed
Publication date: 2024/04/18
Sanli FatmaTatar ArzuGundogdu BetulKaratas Omer Faruk - KRas-induced actin-interacting protein (KRAP) has been identified as crucial for the appropriate localization and functioning of the inositol trisphosphate receptors (IPRs) that mediate Ca release from the endoplasmic reticulum. Here, we used siRNA knockdown of KRAP expression in HeLa and HEK293 cells to examine the roles of KRAP in the generation of IP-mediated local Ca puffs and global, cell-wide Ca signals. High resolution Ca imaging revealed that the mean amplitude of puffs was strongly reduced by KRAP knockdown, whereas the Ca flux during openings of individual IPR channels was little affected. In both control and KRAP knockdown cells the numbers of functional channels in the clusters underlying puff sites were stochastically distributed following a Poisson relationship, but the mean number of functional channels per site was reduced by about two thirds by KRAP knockdown. We conclude that KRAP is required for activity of IPR channels at puff sites and stochastically 'licenses' the function of individual channels on a one-to-one basis, rather than determining the functioning of the puff site as a whole. In addition to puff activity ('punctate' Ca release), global, cell-wide Ca signals evoked by higher levels of IP are further composed from a discrete 'diffuse' mode of Ca release. By applying fluctuation analysis to isolate the punctate component during global Ca signals, we find that KRAP knockdown suppresses to similar extents punctate and diffuse Ca release in wild-type cells and in HEK293 cells exclusively expressing type 1 and type 3 IP3Rs. Thus, KRAP appears essential for the functioning of the IPRs involved in diffuse Ca release as well as the clustered IPRs that generate local Ca puffs. - Source: PubMed
Publication date: 2022/08/19
Vorontsova IreneLock Jeffrey TParker Ian