Synthetic with Lin-35/Rb 2

abnormal cell LINeage 33

abnormal cell LINeage 38

abnormal cell LINeage 31

abnormal cell LINeage 3

abnormal cell LINeage 32

abnormal cell LINeage 35

abnormal cell LINeage 37

abnormal cell LINeage 36

abnormal cell LINeage 39

Motor neuron (MN) diversity is essential for generating animal movement, yet the molecular mechanisms specifying MN subtypes remain poorly understood. We investigate how Hox genes and their PBX co-factors establish cholinergic MN identity along the a...

Chronic exposure to low concentrations of polystyrene nanoparticles (PS-NPs) can induce reproductive toxicity across multiple generations, yet the underlying molecular mechanisms remain poorly defined. Our previous studies showed that the parental ge...

Cytoplasmic phospholipase A2 (PLA2) is known to be phosphorylated and activated by MAP kinase (Lin et al 1993, Cell 72: 269-278), an important downstream component of signal transduction, whereas paclitaxel has been shown to inhibit isoprenylation of...

As transcription factors of the lines (LIN)-11/Islet (Isl)-1/mitosis entry checkpoint (MEC)-3 (LIM)-homeobox subfamily, LIM homeobox (Lhx)6 and -8 are remarkably conserved and involved in the morphogenesis of multiple organ systems. Lhx6 and -8 play ...

We have cloned and sequenced two new cDNAs that code for proteins carrying the related triple LIM domains (acronym of Lin-11, Isl-1, Mec-3) proteins. These LIM domains show good agreement to the LIM domain consensus sequence, but also exhibit some no...

The oriented peptide library technique was used to investigate the peptide-binding specificities of nine PDZ domains. Each PDZ domain selected peptides with hydrophobic residues at the carboxyl terminus. Individual PDZ domains selected unique optimal...

The derived protein sequence of the presumptive oncogene rhombotin is virtually identical between human and mouse (Boehm et al., 1990), rendering it difficult to identify functionally important regions or motifs. We have therefore sought to isolate a...

Spinal muscular atrophy (SMA) is a motoneuron disease caused by deletions of the Survival of Motoneuron 1 gene (SMN1) and low SMN protein levels. SMN restoration is the concept behind a number of recently approved drugs which result in impressive yet...

To become and remain functional, individual neuron types must select during development and maintain throughout life their distinct terminal identity features, such as expression of specific neurotransmitter receptors, ion channels and neuropeptides....

Macroautophagy/autophagy is essential for maintaining cellular homeostasis through the degradation of organelles and proteins. It also has a prominent role in modulating aging. However, the role of autophagy in the neuronal response to axon injury an...

NH2-PS-NP (10 μg/L) further caused more severe transgenerational activation of germline ligand genes (ins-3, ins-39, daf-28, lin-44, egl-17, efn-3, and lag-2) than PS-NP (10 μg/L), and RNAi of these ligand genes caused resistance to the toxicity of PS-NP and NH2-PS-NP on locomotion and neuronal development.

Furthermore, LIN-3 overexpression transgenerationally enhanced EGF receptor/LET-23 expression in the progeny, and let-23 RNAi in F1-generation notably suppressed PS-A NPs' transgenerational toxicity in the exposed worms overexpressing germline LIN-3 at P0 generation.

In anterior MNs, we show that the anterior Hox genes ceh-13 (Lab/Hox1) and lin-39 (Scr/Dfd/Hox4-5) collaborate with the Hox cofactor ceh-20 (Exd/Pbx1-4) and the terminal selector unc-3 (Collier/Ebf1-4) to activate terminal identity genes.

We found that LIN-24 expression is upregulated during starvation, leading to increased expression of the lipase-encoding gene lipl-3.

The ectodomain of SISS-1 , but not of LIN-3 , also contains an Immunoglobulin-like (Ig) domain, putting it into a class of Ig-EGFs that includes Drosophila Vein and certain vertebrate Neuregulins.

NH2-PS-NP (10 μg/L) further caused more severe transgenerational activation of germline ligand genes (ins-3, ins-39, daf-28, lin-44, egl-17, efn-3, and lag-2) than PS-NP (10 μg/L), and RNAi of these ligand genes caused resistance to the toxicity of PS-NP and NH2-PS-NP on locomotion and neuronal development.

LIN-65 and histone methyltransferase MET-2 then orchestrate the downregulation of lin-3/EGF transcription to repress ras(gf)-driven vulval defects.

In anterior MNs, we show that the anterior Hox genes ceh-13 (Lab/Hox1) and lin-39 (Scr/Dfd/Hox4-5) collaborate with the Hox cofactor ceh-20 (Exd/Pbx1-4) and the terminal selector unc-3 (Collier/Ebf1-4) to activate terminal identity genes.

This induction of germline apoptosis was dependent on known and novel regulators of germline apoptosis including members of the conserved DREAM (Dp, Retinoblastoma (Rb)-like, E2F, MuvB) complex: LIN-35/pRB, LIN-54, and LIN-37, and proteins that regulate the synapsis checkpoint, BUB-3 and PCH-2.

After PS-NP exposure, expressions of ins-3, daf-28, and ins-39 encoding insulin ligands, efn-3 encoding Ephrin ligand, and lin-44 encoding Wnt ligand, as well as expressions of their receptor genes (daf-2, vab-1, and/or mig-1), were dysregulated by the RNAi of daf-12, nhr-14, nhr-47, and nhr-12.