#EIF3D
A new paper from the lab shows that Nanos3 and Dead end1 can form a complex with eIF3d to activate RNA translation in primordial germ cells.
link.springer.com/article/10.1...
A Nanos3-containing protein complex can activate RNA translation in primordial germ cells in vivo - EMBO Reports
Maintaining the germline fate requires tight post-transcriptional control of RNA function. Here, we investigate how primordial germ cell (PGC) identity is maintained in zebrafish and reveal that the c...
link.springer.com
April 24, 2026 at 4:22 PM
3/4 We identify novel substrates like #RPL22, #EIF3D and #PCM1, opening new doors to more functional insights into these #posttranslationalmodifications so far implicated primarily in #microtubule regulation. Their role in #cellbiology seems more than what is thought to be.
June 12, 2026 at 1:50 AM
A CRISPR screen has identified EIF3D as a key regulator of stem cell pluripotency, highlighting its role in protein translation and its impact on maintaining primed pluripotency. doi.org/g9d73r
CRISPR screen identifies EIF3D as critical regulator of stem cell pluripotency maintenance
A team of CiRA researchers has uncovered the crucial role of EIF3D—a protein translational regulator—in primed pluripotency.
phys.org
April 12, 2025 at 3:47 AM
RRIDs were included in this Science Advances paper. We value the author's support of reproducibility. #accelerateopenscience #accelerateopenscience #accelerateopenscience
EIF3D safeguards the homeostasis of key signaling pathways in human primed pluripotency
doi.org
May 21, 2025 at 7:00 AM
A paper using RRID:AB_10666428 from @proteintech.bsky.social was just published. Thanks for making your methods matter! #OpenScience #reproducibility #ReproducibleResearch
eIF3d and eIF3e mediate selective translational control of hypoxia that can be inhibited by small molecules
doi.org
December 10, 2025 at 8:00 AM
In other words, eIF3d phosphorylation helps translation initiation through eIF4F, and indeed, in human cells, it modulates the strength of interaction between the two complexes (as shown by Nick Roiuk @mykolaroiuk.bsky.social and Aurelio Teleman @telemanlab.bsky.social )
March 12, 2025 at 3:22 PM
This led us to a new hypothesis as to how eIF3d works: whereas previous work showed it is responsible for binding the cap when eIF4F is absent, in our situation, eIF3d phosphorylation and eIF4F act together to maintain stem cell fate.
March 12, 2025 at 3:22 PM
We focused on one of the regulators we identify in the screen: eIF3d. Previous work by Amy Lee and colleagues showed that eIF3d is regulated by phosphorylation, by a kinase called CK2. Knockdown of CK2 also leads to loss of stem cells, similar to loss of eIF3d and eIF4F.
March 12, 2025 at 3:22 PM
Elegant and impactful work on how a translation-dependent splicing program, downstream of Myc, controls breast cancer plasticity!! Congratulations Cristian, Ana and team!! ⁦@BellodiCristian⁩ ⁦@ana_bosch79⁩ ⁦@CieslaMaciej⁩

cell.com/molecular-cell…
Oncogenic translation directs spliceosome dynamics revealing an integral role for SF3A3 in breast cancer
Cieśla et al. uncover a translation-based regulatory layer that steers central spliceosome nodes following oncogenic stress. eIF3D-mediated SF3A3 translation provides an exquisite mechanism to enable cancer-promoting alternative splicing patterns downstream of MYC hyperactivation. This critically rewires cancer cell metabolism and plasticity, highlighting a role for SF3A3 in human breast cancers.
www.cell.com
March 24, 2025 at 12:55 AM
eIF3d and eIF3e mediate selective translational control of hypoxia that can be inhibited by novel small molecules https://www.biorxiv.org/content/10.1101/2025.05.29.656739v1
May 29, 2025 at 2:48 PM
eIF3d and eIF3e mediate selective translational control of hypoxia that can be inhibited by novel small molecules https://www.biorxiv.org/content/10.1101/2025.05.29.656739v1
May 29, 2025 at 2:48 PM
PXD053390 🚨

Asymmetric dimethylarginine (aDMA) at the N-terminal of eIF3D plays a regulatory role in protein translation initiation.

🚨 New dataset alert! 🚨
December 24, 2025 at 11:00 AM