KIF23 antibody - middle region (ARP33910_P050)
- Known as:
- KIF23 (anti-) - middle region (ARP33910_P050)
- Catalog number:
- arp33910_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- KIF23 antibody - middle region (ARP33910_P050)
Ask about this productRelated genes to: KIF23 antibody - middle region (ARP33910_P050)
- Gene:
- KIF23 NIH gene
- Name:
- kinesin family member 23
- Previous symbol:
- KNSL5
- Synonyms:
- MKLP1, MKLP-1
- Chromosome:
- 15q23
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-07
- Date modifiied:
- 2019-04-23
Related products to: KIF23 antibody - middle region (ARP33910_P050)
Related articles to: KIF23 antibody - middle region (ARP33910_P050)
- Metamorphosis is a critical ontogenetic transition for marine bivalves, marking the shift from planktonic to benthic lifestyles, where successful transformation dictates survival. The razor clam Sinonovacula constricta is economically important; however, low larval metamorphosis rates remain a major bottleneck in seedling production. To elucidate the mechanisms governing this process, we performed a comparative transcriptome analysis of S. constricta larvae at pre- and post-metamorphosis stages using Illumina sequencing. A total of 3701 differentially expressed genes (DEGs) were identified, including 3254 up-regulated and 447 down-regulated genes. Functional annotation of the respective top 20 significantly up-regulated and down-regulated DEGs indicated their potential pivotal roles in signal transduction (e.g., up-regulated: CAV1, CHRNA2; down-regulated: APP, NOTCH1), cellular proliferation and differentiation (e.g., up-regulated: TUBA, EGF1; down-regulated: KIF23, TTC25), transcriptional and epigenetic regulation (e.g., up-regulated: NFIL3; down-regulated: OVO, HMX1), substance transport (e.g., up-regulated: LRP2, LRP1B; down-regulated: SLC51A, Slc33a1), substance metabolism (e.g., up-regulated: CPK3, CYP26A1; down-regulated: RDMT1, ADAC), immunomodulation (e.g., up-regulated: CPN2, CRISP2), and protein homeostasis (e.g., up-regulated: HSP27, NAS-27). Functional enrichment analysis further revealed that DEGs were significantly enriched in pathways related to signal transduction and developmental regulation (e.g., Ras, TNF), cell death and homeostasis (e.g., apoptosis), immune responses (e.g., Toll-like receptor), energy metabolism (e.g., lipid), cardiovascular related (e.g., Fluid shear stress), cell junction and architecture (e.g., Tight junction), and infectious disease (e.g., measles). These results suggest a synergistic interplay between signaling, apoptosis, immunity, and metabolism during S. constricta metamorphosis. This study advances our understanding of marine bivalve metamorphosis and offers candidate genes for further mechanistic studies. - Source: PubMed
Publication date: 2026/08/14
Zhou QiangKong FeiLi DechengRan ZhaoshouXu Jilin - Doxorubicin-induced cardiomyopathy (DIC) is a common and severe cardiotoxic effect of doxorubicin (DOX)-based chemotherapy. This study aimed to identify core genes associated with DIC and investigate their immunoregulatory mechanisms. - Source: PubMed
Publication date: 2026/08/01
Xiao DabaoZhang ZhuoXiao XinDeng WenyiZeng MengyaXiao ShaowuZou ShihaoChen RichaoChen Yuewu - Long noncoding RNAs (lncRNAs) have emerged as important modulators in the molecular pathology of cancer. lncRNA ABCA9-AS1 is a newly identified lncRNA, and its role in gastric cancer has not yet been reported. - Source: PubMed
Publication date: 2026/07/22
Wu YiwenXia YiniuLiu HanyuWen ShilinZhong KemingXiao QianwenWang ZhouYang XiaoyanXie Zhizhong - - Source: PubMed
Publication date: 2026/07/22
Wang XiaoxiaoWang WeiZeng HanlingHu XinruChen FangyiShen LiTao Jing - Thyroid cancer (TC) is the most common endocrine malignancy, with incidence increasing worldwide. Although most differentiated TCs have a favorable prognosis, radioiodine (RAI)-refractory differentiated thyroid cancer (DTC), BRAF inhibitor-resistant papillary thyroid cancer, and anaplastic thyroid cancer (ATC) remain major areas of unmet clinical need. The sirtuin (SIRT) family of NAD-dependent enzymes has emerged as a multifaceted regulator of TC biology, with isoform-specific dichotomous roles: SIRT1, SIRT6, and SIRT7 act as tumor promoters through engagement of BRAF/MAPK, PI3K/AKT, epithelial-mesenchymal transition (EMT), and Hippo pathways, while SIRT3 and SIRT4 function as tumor suppressors via mitochondrial metabolic regulation. This review synthesizes recent developments that expand the therapeutic landscape: (i) the recognition that SIRT7 functions as a desuccinylase with preclinically identified oncogenic substrates, modifying KIF23 in ATC and LATS1 in PTC; (ii) the emerging roles of isoform-specific SIRT axes, including the NAMPT-SIRT1-PD-L1 axis, SIRT6-associated regulatory T-cell biology, and SIRT2 as a T-cell metabolic checkpoint, as determinants of immune microenvironment state and potential modulators of immune checkpoint inhibitor response; and (iii) the SIRT6-nuclear receptor coactivator 4 (NCOA4) ferritinophagy axis as a supported ferroptosis vulnerability in ATC, with potential but still hypothesis-generating relevance to dedifferentiated and RAI-refractory DTC. Importantly, the therapeutic logic for SIRT6 is disease-state-specific rather than contradictory: SIRT6 inhibition is rationalized in BRAF-driven aggressive PTC and DTC contexts where SIRT6 supports MAPK signaling, EMT, and ferroptosis resistance, whereas in SIRT6-high ATC, the same enzyme's NCOA4-dependent ferritinophagy activity may instead be exploited to enhance ferroptosis sensitivity. We review the current SIRT modulator pharmacological toolkit-including EX-527, OSS_128167, and emerging SIRT7-selective inhibitors-and identify the substantial clinical translation gap, with no SIRT-targeted clinical trial yet conducted in TC, despite strong preclinical rationale. We outline biomarker-stratified combination strategies with BRAF/MEK inhibitors, multikinase inhibitors, immune checkpoint inhibitors, and ferroptosis inducers, prioritizing biomarker-driven preclinical validation and, where supported by efficacy and safety data, subsequent early-phase evaluation in V600E-mutant and SIRT6-high thyroid cancer. Sirtuins thus represent a mechanistically promising and potentially biomarker-stratifiable therapeutic hypothesis for difficult-to-treat thyroid cancer; however, clinical translation remains at an early stage and requires validated biomarkers, isoform-selective compounds, and disease-specific in vivo evidence. - Source: PubMed
Publication date: 2026/06/27
Cho Ki JuSeo Ji HyunKwon HayeongLee Seung-JunHah Young-SoolPark Jung Je