Ask about this productRelated genes to: PIM2 antibody
- Gene:
- PIM2 NIH gene
- Name:
- Pim-2 proto-oncogene, serine/threonine kinase
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- Xp11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-26
- Date modifiied:
- 2015-09-04
Related products to: PIM2 antibody
Related articles to: PIM2 antibody
- Innate immune dysregulation is increasingly recognized as a pivotal contributor to hypertension pathogenesis. However, the role of natural killer (NK) cells, a key innate lymphocyte population, remains poorly defined and controversial. - Source: PubMed
Publication date: 2026/04/16
Wang XiaoqiYang QiaoxiBian JinFan LuyunZhao XueyanCai Jun - Cyclin D1 (CCND1) as a regulator of the cell cycle has been implicated in disease progression and prognosis of human malignancies. However, its prognostic significance in cytoplasmic versus nuclear localizations has not been well established in human prostate cancer (PCa). - Source: PubMed
Publication date: 2026/04/27
Ayala AlejandroDing YiBu PingMiles BrianAyala Gustavo - - Source: PubMed
Publication date: 2026/04/21
Zhang ZongyeWang HongboCheng XingboZhang ZhichangHou ZhenxingLiu ZhendongGao Yanzheng - Ustekinumab is a monoclonal antibody therapy targeting interleukin-12 and interleukin-23 for the treatment of inflammatory bowel diseases, including ulcerative colitis (UC). While these pathways remain quite attractive for UC therapy, response to ustekinumab can be variable. There is an urgent need to better understand the underlying mucosal immune alterations associated with treatment to guide therapy decisions. This study aims to examine the mucosal immune signatures in individuals with UC with variable treatment response to ustekinumab. - Source: PubMed
Publication date: 2026/04/15
Briggs Kristi CTam AdaChaaban LaraLuo AdamKobeissi LynnLazarev MarkParian AlyssaChowdhury ReezwanaSelaru Florin MCasella KellyShenderov EugeneSears Cynthia LHousseau FranckMelia Joanna M PPardoll Drew M - The oncogenic fusion protein NPM-ALK drives anaplastic large cell lymphoma (ALCL) by activating the transcription factor STAT3. While STAT3 phosphorylation at Y705 and S727 is well characterized, the present study defines a mechanistic role for phosphorylation at T714 in supporting full STAT3 functionality. In NPM-ALK-positive ALCL cells, STAT3 is phosphorylated at Y705, S727, and T714, and this is suppressed by ALK inhibition. Enforced NPM-ALK expression in Ba/F3 cells induces phosphorylation at all three sites in a kinase-dependent manner. To investigate the role of T714, wild-type STAT3 or a T714A mutant was reconstituted into STAT3-knockdown Ba/F3 cells expressing NPM-ALK. Wild-type STAT3 underwent Y705 and S727 phosphorylation and nuclear translocation, whereas the T714A mutant was phosphorylated at S727 only and failed to translocate. The reduced expression of STAT3 target genes (Cyclin D1, Pim1, Pim2, and Socs3) with STAT3 knockdown was restored by wild-type STAT3, but not by the T714A mutant. In vivo, STAT3 knockdown suppressed tumor formation and hepatosplenomegaly in mice inoculated with Ba/F3 cells expressing NPM-ALK, and these phenotypes were rescued by wild-type STAT3, but not by the T714A mutant. These findings indicate that STAT3 phosphorylation at T714 is required for subsequent Y705 phosphorylation, nuclear translocation, and transcriptional activation specifically within the context of NPM-ALK-mediated signaling. - Source: PubMed
Publication date: 2026/03/25
Lin XinYao YoshiyukiMoriwaki YasuhiroTago KenjiFunakoshi-Tago Megumi