Cobalt recycling patents dataset selected using 'green' classification codes: Focus on the nickel manganese cobalt (NMC) batteries recycling.

The Critical Raw Materials Act has been emanated to address perceived risks around supply chains for critical raw materials in light of expected demand growth [1]. Cobalt is one of the critical raw materials for the EU: it plays a central role in transition to a low-carbon economy and is crucial for batteries powering electric vehicles. The cobalt industry is important not only because of the green transition, it also creates employment opportunities as Europe is the third largest region for total global cobalt value chain employment [2].

Downregulation of Akt activity contributes to the growth arrest induced by FGF in chondrocytes.

Unregulated FGF signaling produced by activating FGFR3 mutations causes several forms of dwarfism-associated chondrodysplasias in humans and mice. FGF signaling inhibits chondrocyte proliferation by activating multiple signal transduction pathways that all contribute to chondrocyte growth arrest and induction of some aspects of differentiation. Previous studies had identified the Stat1 pathway, dephosphorylation of the Rb family proteins p107 and p130, induction of p21 expression and sustained activation of MAP kinases as playing a role in the FGF response of chondrocytes.

A network of transcriptional and signaling events is activated by FGF to induce chondrocyte growth arrest and differentiation.

Activating mutations in FGF receptor 3 (FGFR3) cause several human dwarfism syndromes by affecting both chondrocyte proliferation and differentiation. Using microarray and biochemical analyses of FGF-treated rat chondrosarcoma chondrocytes, we show that FGF inhibits chondrocyte proliferation by initiating multiple pathways that result in the induction of antiproliferative functions and the down-regulation of growth-promoting molecules. The initiation of growth arrest is characterized by the rapid dephosphorylation of the retinoblastoma protein (pRb) p107 and repression of a subset of E2F target genes by a mechanism that is independent of cyclin E-Cdk inhibition.