Multiple domains of the integral KREPA3 protein are critical for the structure and precise functions of RNA editing catalytic complexes in .

The gRNA directed U-insertion and deletion editing of mitochondrial mRNAs that is essential in different life-cycle stages for the protozoan parasite is performed by three similar multiprotein catalytic complexes (CCs) that contain the requisite enzymes. These CCs also contain a common set of eight proteins that have no apparent direct catalytic function, including six that have an OB-fold domain. We show here that one of these OB-fold proteins, KREPA3 (A3), has structural homology to other editing proteins, is essential for editing, and is multifunctional.

Multiple domains of the integral KREPA3 protein are critical for the structure and precise functions of RNA Editing Catalytic Complexes in .

The gRNA directed U-insertion and deletion editing of mitochondrial mRNAs that is essential in different life cycle stages for the protozoan parasite is performed by three similar multi-protein catalytic complexes (CCs) that contain the requisite enzymes. These CCs also contain a common set of eight proteins that have no apparent direct catalytic function, including six that have an OB-fold domain. We show here that one of these OB-fold proteins, KREPA3 (A3), has structural homology to other editing proteins, is essential for editing and is multifunctional.

Pandemic-Related Instructor Talk: How New Instructors Supported Students at the Onset of the COVID-19 Pandemic.

At the same time that COVID-19 cases in the United States first began to increase, fellows in a mentored teaching apprenticeship for postdoctoral scientists began to teach undergraduate seminars. The fellows suddenly needed to support students emotionally and switch to online instruction. They were encouraged to acknowledge and address the pandemic during each class and decided to do so.

Cul3 regulates cyclin E1 protein abundance via a degron located within the N-terminal region of cyclin E.

Cyclin E and its binding partner Cdk2 control the G1/S transition in mammalian cells. Increased levels of cyclin E are found in some cancers. Additionally, proteolytic removal of the cyclin E N-terminus occurs in some cancers and is associated with increased cyclin E-Cdk2 activity and poor clinical prognosis.

Hyperkalemic hypertension-associated cullin 3 promotes WNK signaling by degrading KLHL3.

Familial hyperkalemic hypertension (FHHt) is a monogenic disease resulting from mutations in genes encoding WNK kinases, the ubiquitin scaffold protein cullin 3 (CUL3), or the substrate adaptor kelch-like 3 (KLHL3). Disease-associated CUL3 mutations abrogate WNK kinase degradation in cells, but it is not clear how mutant forms of CUL3 promote WNK stability. Here, we demonstrated that an FHHt-causing CUL3 mutant (CUL3 Δ403-459) not only retains the ability to bind and ubiquitylate WNK kinases and KLHL3 in cells, but is also more heavily neddylated and activated than WT CUL3.

Novel Cul3 binding proteins function to remodel E3 ligase complexes.

Background: Cullins belong to a family of scaffold proteins that assemble multi-subunit ubiquitin ligase complexes to recruit protein substrates for ubiquitination via unique sets of substrate adaptor, such as Skp1 or Elongin B, and a substrate-binding protein with a conserved protein-protein interacting domain, such as leucine-rich repeats (LRR), a WD40 domain, or a zinc-finger domain. In the case of the Cullin3 (Cul3), it forms a BTB-Cul3-Rbx1 (BCR) ubiquitin ligase complex where it is believed that a BTB domain-containing protein performs dual functions where it serves as both the substrate adaptor and the substrate recognition protein.

Results: Tandem affinity purification and LC/MS-MS analysis of the BCR complex led to the identification of 10,225 peptides.

Amorphous alumina nanowire array efficiently delivers Ac-DEVD-CHO to inhibit apoptosis of dendritic cells.

To create an effective well-ordered delivery platform still remains a challenge. Herein we fabricate vertically aligned alumina nanowire arrays via atomic layer deposition templated by carbon nanotubes. Using these arrays, a caspase-3/7 inhibitor was delivered into DC 2.