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loss of Llgl1 results in EGFR (Montrer EGFR Protéines) mislocalization, promoting pre-neoplastic changes
these results revealed that miR (Montrer MLXIP Protéines)-652-3p execute a tumor-promoter function in non-small cell lung cancer through direct binding and regulating the expression of Lgl1 (Montrer CRISPLD2 Protéines)
Older age is a strong predictor of CNS involvement in patients seropositive for CASPR2 (Montrer CNTNAP2 Protéines)-IgG or LGI1 (Montrer LGI1 Protéines)-IgG. Pain, peripheral manifestations, and stereotypic paroxysmal dizziness spells are common with LGI1 (Montrer LGI1 Protéines)-IgG.
Reduced expression of Hugl 1 predicts poor survival in lung SqCC patients. The expression of Hugl 1 was inversely correlated with both overall survival rate and tumor stage.
Our results support the growing appreciation that the tumour regulatory functions of Scribble (Montrer SCRIB Protéines), and other polarity protein family members, are context dependent.
this study provides the evidence that Hugl-1 inhibits glioma cell growth in intracranial model of nude mice, suggesting that Hugl-1 might be a potential tumor target for glioma therapy.
Lgl1 (Montrer CRISPLD2 Protéines) has a role in inhibiting glioblastoma
PTEN loss leads to the phosphorylation and inactivation of Lgl by atypical protein kinase C (Montrer PRKCZ Protéines) in glioblastoma cells.
Suggest that Hugl-1 induces growth suppression and apoptosis in a human esophageal squamous cell carcinoma cell line both in vitro and in vivo.
inactivation of Llgl1 enhances hematopoietic stem cells self-renewal and fitness and is associated with unfavorable outcome in human acute myeloid leukemia (Montrer BCL11A Protéines)
Ablation of Llgl1 gene Results in Severe Brain Malformation.
Lgl1 (Montrer Klra7 Protéines) is required for the development of the olfactory bulb.
results suggest that neural stem cell-mediated neuron and glia production is tightly regulated through the concerted interplay of sequential Lgl1 (Montrer Klra7 Protéines)-dependent global and cell intrinsic mechanisms.
These results reveal a novel role for Lgl-1 (Montrer Klra7 Protéines) in the regulation of virus-specific T-cell responses and antitumor immunity.
Data indicate hyperproliferation, impaired differentiation and increased apoptosis of neural progenitors in the cerebellum of lethal giant larvae homolog 1 (Lgl1 (Montrer Klra7 Protéines))-Pax2 (Montrer PAX2 Protéines) protein knockout embryos.
Lgl1 (Montrer Klra7 Protéines) forms two distinct complexes in vivo, Lgl1 (Montrer Klra7 Protéines)-NMIIA and Lgl1 (Montrer Klra7 Protéines)-Par6alpha (Montrer PARD6A Protéines)-aPKCzeta (Montrer PRKCZ Protéines), and that the formation of these complexes is affected by the phosphorylation state of Lgl1 (Montrer Klra7 Protéines).
Collectively these findings indicate that Lgl1 (Montrer Klra7 Protéines) regulates the polarity of migrating cells by controlling the assembly state of NMII-A, its cellular localization, and focal adhesion assembly.
This is the first study to demonstrate the involvement of Dlg1 (Montrer DLG1 Protéines), Scrib (Montrer SCRIB Protéines), and Lgl1 (Montrer Klra7 Protéines) in a mouse with ocular adenocarcinoma and the simultaneous involvement of these proteins in the same cancer.
Findings reveal that RanBPM plays a novel role in regulating Mgl-1 stability and contributes to its biological function as a tumor suppressor.
mgl-1 mRNA is developmentally expressed in CNS, craniofacial region, eyes, limbs, and the gut (Montrer GUSB Protéines)
This gene encodes a protein that is similar to a tumor suppressor in Drosophila. The protein is part of a cytoskeletal network and is associated with nonmuscle myosin II heavy chain and a kinase that specifically phosphorylates this protein at serine residues. The gene is located within the Smith-Magenis syndrome region on chromosome 17.
disks large homolog 4
, lethal(2) giant larvae protein homolog 1
, human homolog to the D-lgl gene protein