The present invention is directed to compositions comprising modified SMARCB1 and uses thereof.

Described herein are methods of characterizing agent incorporation into condensates, methods of reducing transcription of oncogenes associated with condensates, and methods of using peptides to inhibit nuclear receptor and cofactor binding in condensates.

Provided are peptides that based on the amino acid sequences LDPAKDCGDQKYAY (SEQ ID NO: 1) and LDPSKDCGDPKYAY (SEQ ID NO: 2), optionally wherein the peptide includes an N-terminal stearate modification. Also provided are method for using the disclosed peptides for inhibiting neointima formation in mammals, methods for inhibiting division and/or proliferation of vascular smooth muscle cells, and uses of the disclosed peptides for treating cardiovascular diseases and/or disorder associated with undesirable vascular SMC proliferation, which in some embodiments can re-late to inhibiting neointima formation in a mammal.

The present invention concerns methods to identify RIPK1 modulators capable of modulating RIPK1 activity, RIPK1 interacting molecules that modulate RIPK1 activity and pharmaceutical compositions comprising RIPK1 modulators.

Compositions, methods, and kits are provided for assaying calpain-5 activity and inhibition. In particular, novel peptide substrates are provided for detecting calpain-5, measuring calpain-5 activity, and screening for inhibitors of calpain-5 to identify potential therapeutic agents for treating retinal diseases and other diseases associated with calpain-5 hyperactivity. Additionally, novel inhibitors of calpain-5 are also provided.

Genetically encoded calcium indicator (GECI) polypeptides and the nucleic acid molecules encoding such polypeptides are provided.

Disclosed are compositions and methods for treating disease or condition caused or exacerbated by S100A9 activity, such as myelodysplastic syndromes (MDS) using a composition comprising an effective amount of a CD33/S100A9 inhibitor.

The invention relates to methods of identifying compounds that modulate mTORC1 activity in a cell by modulating the activity of SAMTOR, as well as to the use of such identified compounds in the modulation of mTORC1 and the treatment of diseases and conditions characterized by aberrant mTORC1 activity.

A method for quantifying the activity of the proteins/enzymes involved in the conjugation of the SUMO/Ubiquitin/Nedd8 proteins in a cell of a biological sample the method including: a) a step of contacting a cellular extract of cell with each protein of a subgroup of at least 3 proteins wherein the at least 3 proteins corresponds to the proteins essentially including or only including the sequences SEQ ID NO: 1 to 3, b) a step of simultaneously measuring ubiquitination, sumoylation and neddylation level of each of the at least 3 proteins to obtain a first value for ubiquitin, SUMO and Nedd8.

The present invention resides in the discovery that the specific interaction between Myeloid Differentiation factor 2 (MD2) and integrin, especially integrin αvβ3, is involved in cellular signaling mediated by MD2-integrin, such as inflammatory response including sepsis. Thus, this invention provides for a novel method for inhibiting integrin signaling by using an inhibitor of MD2-integrin binding, such as a dominant negative mutant of MD2 without integrin-binding capability. A method for identifying inhibitors of MD2-integrin binding is also described. Further disclosed are polypeptides, nucleic acids, host cells, and corresponding compositions for inhibiting MD2-integrin signaling.