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that the reduced expression of LimD1 and VHL (show VHL Proteins) might have synergistic effect on induction of HIF1alpha (show HIF1A Proteins) resulting increased cellular proliferation and progression of the disease.
our data also suggests the importance ofLIMD1 and CDC25A (show CDC25A Proteins) in conjunction with HPV for use as diagnostic and prognostic markers of HNSCC, whereas RBSP3 (show CTDSPL Proteins) as a prognostic marker only.
LIMD1 coordinates the assembly of an AGO-TNRC6 containing miRISC complex by binding both proteins simultaneously at distinct interfaces.
These results suggested that LIMD1 is a novel BRCA2-interacting protein and is involved in the centrosome localization of BRCA2 (show BRCA2 Proteins) and suppression of LIMD1, causing abnormal cell division in EC cells.
Thus, the LIMD1-MYBL1 (show MYBL1 Proteins) Index had considerable clinical value for DLBCL subtype classification and prognosis.
Cyclic stretch is associated with a JNK (show MAPK8 Proteins)-dependent increase in binding of a LATS inhibitor, LIMD1, to the LATS1 kinase and that reduction of LIMD1 expression suppresses the activation of YAP (show YAP1 Proteins) by cyclic stretch.
LIMD1 prevents retinoblastoma phosphorylation and downregulates of E2F1 (show E2F1 Proteins) protein and blocks entry of cells into S-phase.
Data show that the tumour suppressor protein LIMD1 acts as a molecular scaffold, simultaneously binding the PHDs and VHL (show VHL Proteins), thereby assembling a PHD (show PDC Proteins)-LIMD1-VHL (show VHL Proteins) protein complex and creating an enzymatic niche that enables efficient degradation of HIF-1alpha (show HIF1A Proteins).
PU.1 is a major transcriptional activator of LIMD1
LIMD1 inactivation as primary event than inactivation of RB1 (show RB1 Proteins) in head and neck squamous cell carcinoma development.
Limd1 regulates AP-1 (show JUN Proteins) activation through an interaction with Traf6 (show TRAF6 Proteins) to influence osteoclast development
Limd1 influences not only stress osteoclastogenesis but also osteoblast function and osteoblast progenitor commitment. Together, these data identify Limd1 as a novel regulator of both bone osetoclast and bone osteoblast development and function.
Adapter or scaffold protein which participates in the assembly of numerous protein complexes and is involved in several cellular processes such as cell fate determination, cytoskeletal organization, repression of gene transcription, cell-cell adhesion, cell differentiation, proliferation and migration. Positively regulates microRNA (miRNA)-mediated gene silencing and is essential for P-body formation and integrity. Acts as a hypoxic regulator by bridging an association between the prolyl hydroxylases and VHL enabling efficient degradation of HIF1A. Acts as a transcriptional corepressor for SNAI1- and SNAI2/SLUG- dependent repression of E-cadherin transcription. Negatively regulates the Hippo signaling pathway and antagonizes phosphorylation of YAP1. Inhibits E2F-mediated transcription, and suppresses the expression of the majority of genes with E2F1- responsive elements. Regulates osteoblast development, function, differentiation and stress osteoclastogenesis. Enhances the ability of TRAF6 to activate adapter protein complex 1 (AP-1) and negatively regulates the canonical Wnt receptor signaling pathway in osteoblasts. May act as a tumor suppressor by inhibiting cell proliferation (By similarity).
LIM domain-containing protein 1
, LIM domains-containing protein 1