anti-V-Mos Moloney Murine Sarcoma Viral Oncogene Homolog (MOS) Antibodies

Zebrafish V-Mos Moloney Murine Sarcoma Viral Oncogene Homolog (MOS) interaction partners

1. while cyclin B1 RNA granules were disassembled in a manner dependent on actin filament depolymerization, certain fractions of mos RNA granules were disassembled independently of actin filaments. These results suggest that cytoplasmic regulation of translationally repressed mRNAs by formation of different RNA granules is a key mechanism for translational control of

2. employed genetic linkage analysis and physical mapping to place the mosm188 mutation on chromosome 6 in the vicinity of the foxd3 gene

Mouse (Murine) V-Mos Moloney Murine Sarcoma Viral Oncogene Homolog (MOS) interaction partners

1. In Xenopus oocytes, the N-terminal Pro of murine & Xenopus c-MOS is dispensable for degradation if Ser-2 of c-MOS is replaced by a small non-phosphorylatable residue. The N-terminal Pro residue is not a recognition determinant for a ubiquitin ligase.

2. Mos protein is unstable in early mouse embryos

3. This suggests that c-mos might play important roles in spermatogenesis

4. Cdc2 and Mos regulate Emi2 stability to promote the meiosis I-meiosis II transition

Xenopus laevis V-Mos Moloney Murine Sarcoma Viral Oncogene Homolog (MOS) interaction partners

1. Mos is responsible for the mitotic activation of the p42 MAPK pathway in Xenopus egg extracts.

2. Results suggest that the specific synthesis of either B-type cyclins or c-Mos, induced by progesterone, is required to induce meiotic maturation and Cdc2 activation.

3. Thus, Mos and Erp1 collaboratively establish and maintain metaphase II arrest in Xenopus eggs

4. results clarify the direct link of the classical Mos-MAPK pathway to Erp1 in meiotic arrest of vertebrate oocytes

Human V-Mos Moloney Murine Sarcoma Viral Oncogene Homolog (MOS) interaction partners

1. approach identified 18 kinase and kinase-related genes whose overexpression can substitute for EGFR in EGFR-dependent PC9 cells, and these genes include seven of nine Src family kinase genes, FGFR1, FGFR2, ITK, NTRK1, NTRK2, MOS, MST1R, and RAF1.

2. High methylation level in MOS is associated with intestinal metaplasia.

3. among the candidate genes, DNA methylation of MOS may reflect the duration of H. pylori exposure and may be a marker for the development of gastric cancer.

4. In the absence of p53, Mos knockdown prevents multipolar mitoses and exerts genome-stabilizing effects.

5. multiple meiotic genes are aberrantly activated during mitotic catastrophe in p53 mutated lymphoma cells after irradiation; the coordinated expression of MOS and REC8 regulate the extent of arrested mitoses and polyploidy

6. Mos 3' UTR regulatory differences underlie species-specific temporal patterns of Mos mRNA cytoplasmic polyadenylation and translational recruitment during oocyte maturation.

7. Cdc2 and Mos regulate Emi2 stability to promote the meiosis I-meiosis II transition

8. These results clarify the direct link of the classical Mos-MAPK (mitogen-activated protein kinase) pathway to Erp1 in meiotic arrest of vertebrate oocytes.

9. the Mos/MAPK pathway is not essential for initiating goldfish oocyte maturation despite its general function as a cytostatic factor (CSF).

Pig (Porcine) V-Mos Moloney Murine Sarcoma Viral Oncogene Homolog (MOS) interaction partners

1. the length of the MOS 3'-UTR tightly controls the level of translation during oocyte maturation. two U-rich (U5A) elements and the hexanucleotide signal (AAUAAA) are required for translation.