ther plant RLK’s candidate inhibitory proteins have indeed been identified, such as BKI1 or protein phosphate 2A for BRI1. Dephosphorylation of specific residues essential for phosphorylation activity has also been proposed to MedChemExpress CF-101 deactivate RLK’s. A possible candidate inhibitor of SERK1 is KAPP, the PP2C protein phosphatase. Finally, endoplasmatic reticulum associated protein degradation potentially plays a role during incorporation of SERK1-KD into correctly assembled receptor complexes, because ERAD also is important during biogenesis and quality control of other plant receptor complexes. The next challenge is to elucidate whether and how the above mechanisms contribute to keeping SERK1-KD inactive in planta, until its activity is required. ~~ Despite recent advances in our understanding of megakaryocyte growth and platelet production, thrombocytopenia remains a difficult problem in the clinical management of patients with hematologic malignancies. Thrombopoietin is the major cytokine involved in the normal production of platelets. However, TPO has been relatively unsuccessful in the treatment of these patients, particularly in shortening the “thrombocytopenic window”following therapy. Thus, platelet transfusions remain the primary treatment for thrombocytopenia despite its significant costs and relatively short-lived responses. Because of this, there remains an important clinical need for the development of novel approaches to accelerate platelet recovery following myeloablative therapy or severe marrow injury. It has been over 25 years since the original observations were reported describing the unique ability of protein kinase C agonists to promote megakaryocytic differentiation of primary murine cells. However, these early studies, which examined the effects of PKC agonists on megakaryocytic differentiation of normal hematopoietic progenitors, were carried out before megakaryocyte culture conditions from early CD34+ progenitors had been developed. Furthermore, these early studies were done prior to the cloning of TPO, which has markedly improved the ability to generate megakaryocytes from 
hematopoietic progenitors in vitro. Despite this, hundreds of reports have been published in which PKC agonists have been utilized to study various aspects of megakaryocyte differentiation, primarily in leukemia cell lines with megakaryocytic potential. However, little is known about the megakaryopoietic effects of PKC agonists on primary CD34selected cells grown in well-defined culture conditions or in vivo. Beyond the early hematopoietic precursor stages, one of the late decision points in hematopoietic lineage separation is the bifurcation of erythroid and megakaryocytic lineages from a common precursor, the megakaryocytic-erythroid progenitor . The growth factors most responsible for megakaryocytic and erythroid development, TPO and erythropoietin, respectively, share significant sequence homology and activate many of the same signal transduction pathways. Nevertheless, there is little, if any, reciprocal lineage infidelity during either normal erythroid or megakaryocytic differentiation so that cultures of CD34+ progenitors in EPO gives rise to a relatively pure population of erythroblasts and culture in TPO supports virtually no erythroid growth. The discriminating elements for this divergent differentiation scheme are unknown. One potential candidate is Protein Kinase C. This is a heterogeneous 1 Thrombopoietic Activity of the PKC Agonist Ing