The experimental results suggest that SV2A is the binding site of LEV in the brain and that LEV acts by modulating the function of SV2 a, supporting previous indications that LEv possesses a mechanism of action distinct from that of other antiepileptic drugs.Expand
K, a hematopoietic growth factor obtained from conditioned medium of BALB/c 3T3 fibroblasts that stimulates the proliferation of mast cells and early erythroid progenitors, specifically binds to the c-kit receptor.Expand
It is shown that the soluble form of KL is generated by efficient proteolytic cleavage from a transmembrane precursor, KL-1, and that Sld, a viable steel allele, is shown to encode a biologically active secreted mutant KL protein, indicating an important function for both the soluble and the cell associate form of Kl.Expand
It was concluded that the period of expression of c-kit extends from at least as early as type A2 spermatogonia through type B sperMatogonia and into preleptotene sperMATocytes.Expand
It is shown that W37, Wv and W41 are the result of missense mutations in the kinase domain of the c‐kit coding sequence, which affect the c-kit associated tyrosine kinase to varying degrees.Expand
A mast cell proliferation assay is used to purify a 30 kd protein, designated KL, from conditioned medium of Balb/3T3 fibroblasts to apparent homogeneity and KL stimulates the proliferation of normal bone marrow derived mast cells but not mast cells from W mice, although both normal and mutant mast cells respond similarly to IL‐3.Expand
It is concluded that IL- 33 isoforms activate basophils and mast cells to drive type 2 inflammation in chronic stable asthma, and novel IL-33 inhibitors will need to block all biologically active isoforms.Expand
It is demonstrated that the c-kit associated tyrosine-specific protein kinase is functionally impaired in W/WV mast cells, thus providing a molecular basis for understanding the developmental defects that result from mutations at the W locus.Expand
Nucleotide sequence analysis of mutant complementary DNAs revealed a missense mutation that replaces aspartic acid with asparagine at position 790 in the c-kit protein product, a conserved residue in all protein kinases.Expand
The discovery and structure–activity relationship (SAR) of a novel, small-molecule chemical probe for BET family inhibition that was identified through the application of structure-based fragment assessment and optimization techniques has yielded a potent, selective compound with cell-based activity (PFI-1) that may further add to the understanding of BET family function within the bromodomains.Expand