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Transcriptional activator which may act in mitogen- activated protein kinase signaling pathway.. De plus, nous expédions LBH Protéines (10) et beaucoup plus de produits pour cette protéine.
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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 (Montrer NPC1 Anticorps) cell cycle arrest at the G1/S transition, and LBH can suppress the growth of transplanted NPC (Montrer NPC1 Anticorps) tumors in vivo by downregulating LMP1 (Montrer PDLIM7 Anticorps)-mediated NF-kappaB (Montrer NFKB1 Anticorps) 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 (Montrer CRYAB Anticorps) may inhibit synergistically the transcriptional regulation of p53 (Montrer TP53 Anticorps) and p21 (Montrer CDKN1A Anticorps)
LBH is aberrantly overexpressed in mammary tumors of mouse mammary tumor virus (MMTV)-Wnt1 (Montrer WNT1 Anticorps)-transgenic mice and in aggressive basal subtype human breast cancers that display Wnt (Montrer WNT2 Anticorps)/beta-catenin (Montrer CTNNB1 Anticorps) 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 (Montrer MAPK1 Anticorps) 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 (Montrer RUNX2 Anticorps) and/or VEGF (Montrer VEGFA Anticorps) 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