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Transcriptional activator which may act in mitogen- activated protein kinase signaling pathway.. Additionally we are shipping LBH Proteins (9) and many more products for this protein.
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Low LBH level, caused by a rheumatoid arthritis risk allele, is a risk factor for aggressive fibroblast-like synoviocyte behavior.
The expression levels of LBH mRNA in patients with SLE were significantly decreased compared with those in normal controls (P < 0.001). No significant differences were found between LBH mRNA expression levels and SLE disease activity scores, SNP rs7579944 and rs906868.
LBH normally induces NPC (show NPC1 Antibodies) cell cycle arrest at the G1/S transition, and LBH can suppress the growth of transplanted NPC (show NPC1 Antibodies) tumors in vivo by downregulating LMP1 (show PDLIM7 Antibodies)-mediated NF-kappaB (show NFKB1 Antibodies) transcriptional activity.
LBH is a candidate gene for synovial pathology in rheumatoid arthritis. It is regulated by growth factors and modulates cell growth in primary fibroblast-like synoviocytes.
results showed that the interaction of LBH and alphaB-crystallin (show CRYAB Antibodies) may inhibit synergistically the transcriptional regulation of p53 (show TP53 Antibodies) and p21 (show CDKN1A Antibodies)
LBH is aberrantly overexpressed in mammary tumors of mouse mammary tumor virus (MMTV)-Wnt1 (show WNT1 Antibodies)-transgenic mice and in aggressive basal subtype human breast cancers that display Wnt (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) hyperactivation.
LBH is implicated as a candidate gene for congenital heart disease associated with partial trisomy 2p syndrome
These results suggest that hLBH proteins may act as a transcriptional activator in mitogen-activated protein kinase (show MAPK1 Antibodies) signaling pathway to mediate cellular functions.
These studies indicate that LBH deficiency induces S-phase arrest that, in turn, exacerbates inflammation. Because LBH gene variants are associated with type I diabetes mellitus, systemic lupus erythematosus, RA, and celiac disease, these results suggest a general mechanism that could contribute to immune-mediated diseases.
The WNT-controlled transcriptional regulator LBH is required for mammary stem cell expansion and maintenance of the basal lineage.
during endochondral bone formation, Lbh may negatively regulate vascular invasion and formation of the early ossification center at least in part by interfering with Runx2 and/or VEGF expression
Transcriptional activator which may act in mitogen- activated protein kinase signaling pathway.
, limb bud and heart development homolog
, protein LBH
, limb bud and heart-expressed protein
, cleavage 2 protein