Publications by authors named "V Kaartinen"

Bone morphogenetic proteins are essential for bone regeneration/fracture healing but can also induce heterotopic ossification (HO). Understanding accessory factors modulating BMP signaling would provide both a means of enhancing BMP-dependent regeneration while preventing HO. This study focuses on the ability of the collagen receptor, discoidin domain receptor 2 (DDR2), to regulate BMP activity.

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Malocclusions are common craniofacial malformations that cause quality of life and health problems if left untreated. Unfortunately, the current treatment for severe skeletal malocclusion is invasive surgery. Developing improved therapeutic options requires a deeper understanding of the cellular mechanisms responsible for determining jaw bone length.

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Malocclusions are common craniofacial malformations which cause quality of life and health problems if left untreated. Unfortunately, the current treatment for severe skeletal malocclusion is invasive surgery. Developing improved therapeutic options requires a deeper understanding of the cellular mechanisms responsible for determining jaw bone length.

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Article Synopsis
  • - The study explores how dendritic cells (DCs), important immune cells, develop under the influence of the growth factor Flt3 ligand (Flt3L) and its receptor, using CRISPR-Cas9 technology for genetic analysis.
  • - Genome screenings revealed several key regulators of DC differentiation, highlighting the roles of TSC and GATOR1 complexes in controlling progenitor growth and enabling DC development through mTOR signaling inhibition.
  • - The transcriptional repressor Trim33 was identified as crucial for DC differentiation; its absence led to a significant decrease in DC progenitors and specific types of DCs, while promoting the expression of genes related to inflammation rather than DC development.
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The secondary palate forms from two lateral primordia called the palatal shelves which form a contact in the midline, become adherent at the fusing interface (medial edge epithelia, MEE) and subsequently fuse. The gene encoding transforming growth factor-ß3 () is strongly and specifically expressed in MEE cells. Our previous study suggested that expression is controlled via upstream cis-regulatory elements in and around the neighboring gene.

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