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anti-Human IGFBP5 Antibodies:
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Human Polyclonal IGFBP5 Primary Antibody for ELISA, WB - ABIN5518921
Khullar, Sehgal: Evaluation of CIEP and ELISA in a rodent malaria model. in Indian journal of pathology & microbiology 1990
Show all 4 Pubmed References
Human Polyclonal IGFBP5 Primary Antibody for ELISA, WB - ABIN3042733
Hou, Zhang, Liu, Meng, Qiao: Expressions of IGFBP-5, cFLIP in cervical intraepithelial neoplasia, cervical carcinoma and their clinical significances: a molecular pathology. in Journal of experimental & clinical cancer research : CR 2009
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Study results demonstrated that miR-885 promoted metastasis of colorectal cancer (CRC) in vitro, and that von Willebrand factor (vWF) and IGFBP5 are potential novel target genes of miR-885, indicating that the miR-885/vWF and miR-885/IGFBP5 axes may serve roles in the metastasis of CRC.
Data suggest that IGFBP5 nuclear import is mediated by KPNA5/KPNB1 complex; nuclear localization sequence of IGFBP5 is critical domain in this nuclear translocation. (IGFBP5 = insulin-like growth factor binding protein-5; KPNA5 = karyopherin subunit alpha-5; KPNB1 = karyopherin subunit beta-1/importin-beta)
These results suggest that the C-terminus of IGFBP-5 exerts anti-cancer activity by inhibiting angiogenesis via regulation of the Akt/ERK and NF-kB-VEGF/MMP-9 signaling pathway.
AMP-IBP5 markedly enhanced keratinocyte migration and proliferation. AMP-IBP5-induced keratinocyte activation was mediated by Mrg X1-X4 receptors with MAPK and NF-kappaB pathways.
Factor Xa induced endothelial cell senescence through IGFBP-5.
Co-ordinated and reciprocal alteration in IGFBP-2 and -5 expression may play a role in the acquisition of endocrine resistance in breast cancer.
The findings suggest that miR-140 suppresses colorectal cancer progression and metastasis, possibly through downregulating ADAMTS5 and IGFBP5.
MiR-137 inhibited cell proliferation and migration of vascular smooth muscle cells via targeting IGFBP-5 and modulating the mTOR/STAT3 signaling.
dysregulation of DNMT3A and IGFBP5 is relevant to preeclampsia. Thus, we propose that DNMT3A and IGFBP5 can serve as potential markers and targets for the clinical diagnosis and therapy of preeclampsia.
IGFBP5 promoter and exon-I methylation did not have any differences between tumor and adjacent tissues so that IGFBP5 methylation did not change IGFBP5 gene regulation in breast cancer.
IGFBP5 promoted osteogenic differentiation potentials of periodontal ligament stem cells and Wharton's jelly umbilical cord stem cells via the JNK and MEK/Erk signalling pathways.
Data demonstrate that dysregulation of miR-143-3p:Igfbp5 interactions in satellite cells with age may be responsible for age-related changes in satellite cell function.
Results shed light on the mechanism of IGFBP5 as a potential tumor-suppressor in melanoma progression.
data provide further insights into the role of cellular compartmentalization in IGFBP-5-induced fibrosis
Demethylation of IGFBP5 by Histone Demethylase KDM6B Promotes Mesenchymal Stem Cell-Mediated Periodontal Tissue Regeneration by Enhancing Osteogenic Differentiation and Anti-Inflammation Potentials.
Our results suggest that rs6214 on the IGF1 gene and rs2854744 near the IGFBP3 gene potentially play an important role with ASMI in Taiwanese older adults in a metropolitan area.
Data indicate co-localization of insulin-like growth factor binding proteins IGFBP-4, IGFBP-5 in the syncytiotrophoblast layer of first trimester placental villi as early as 5 weeks of gestational age.
rs4442975 at 2q35 flanks a transcriptional enhancer that physically interacts with the promoter of IGFBP5. Evidence suggests that the g-allele confers increased breast cancer susceptibility through relative downregulation of IGFBP5.
IGFBP5 mRNA expression is a good indicator in clinical outcome of breast cancer patients.
miR-204-5p suppresses IGFBP5 expression by direct binding to the 3' untranslated region.
proliferation of IGFBP5-mutated cancer cells is selectively blocked by IGF-1R inhibitors
Results from mouse models suggest that inhibiting the up-regulation of IGFBP5 expression in peripheral nerves might prevent or slow down diabetic neuropathy disease progression
IGFBP-5 induces its pro-fibrotic effects, at least in part, via DOK5. IGFBP-5 and DOK5 are both increased in systemic sclerosis fibroblasts and tissues and may thus be acting in concert to promote fibrosis.
Igfbp2-5 are expressed in distinct and complementary patterns during cochlear development.
indicate that Igf1 was highly expressed in the mesenchyme, Igf2 and Igf1r were expressed in both the midline epithelium and surrounding mesenchyme, and Igfbp5 was highly expressed in the epithelium.
we have identified a single polymorphic locus that affects skin and lung tumorigenesis and identify Igfbp5 and Igfbp2 as candidate modifier genes of lung tumorigenesis.
investigated the effect of IGFBP5 induction on the progression of liver fibrosis caused by chronic cholangiopathy; expression of IGFBP5 in the Abcb4-/- mice reduces inflammation, oxidative stress, ECM deposition and hepatocyte proliferation, thereby reducing liver fibrosis
c-Src and IL-6 inhibit osteoblast differentiation and integrate IGFBP5 signalling
Defining the disulfide bonds of insulin-like growth factor-binding protein-5 by tandem mass spectrometry with electron transfer dissociation and collision-induced dissociation.
Decreased Cav-1 expression in fibrotic diseases likely leads to increased deposition of IGFBP-5 in the extracellular matrix.
Data indicate that retinal astrocytes enhance the proliferation of cone-like retinoblastoma cells by deploying IGFBP5, a factor that also provides trophic support to the tumor cells' non-neoplastic counterparts.
insulin-like growth factor binding protein 5 is a modulator of tamoxifen resistance in breast cancer
Igfbp5 appears to be up-regulated by activation of Akt1 in beta cells or fibroblasts. Knockout studies indicate Igfbp5 may be involved in regulation of metabolism (e.g., glucose intolerance) and growth (i.e., cell size, organ size, and body size).
the timing of IGF-II expression and regulation of its accessibility by IGFBP-5 may play a role in anterior pituitary differentiation, survival, and/or proliferation
that over-expression of IGFBP-5 can lead to; impaired mammary development, increased expression of the pro-apoptotic molecule caspase-3, increased plasmin generation and decreased expression of pro-survival molecules of the Bcl-2 family
IGFBP-5 protein was greatly increased during days 1-3 of mammary gland involution, when levels of apoptosis are dramatically elevated to remodel the gland after lactation
Specific amino acid substitutions determine the differential contribution of the N- and C-terminal domains of insulin-like growth factor (IGF)-binding protein-5 in binding IGF-I
IGFBP-5 is a potent growth inhibitor and proapoptotic agent in human breast cancer cells via modulation of cell cycle regulation and apoptotic mediators
two of the six serum insulin-like growth factor binding protein-5 quantitative trait loci also showed significant association with total body bone mineral density phenotype
The present study revealed SNPs in exon 1 of IGFBP-5 gene in the Tibet Mini-pig, possibly providing more understanding of the mechanism of miniaturization
IGFBP-5 gene is associated with the variation in meat quality, especially in pH value together with other QTLs on chromosome 15.
Endogenous IGFBP-5 or transiently expressed IGFBP-5-EGFP is localized in the nuclei of VSMCs. It possesses transcription-regulatory activity that is IGF independent.
IGFBP5, an important component of IGF signaling pathway, contributes greatly to bovine muscle cell development. A mechanism that miR-143 can regulate the proliferation and differentiation of bovine MSCs through changing expression of IGFBP5 was elucidated by our study.
This study suggested that that higher level IGFBP-5 expression may have functional significance in lactation persistency.
follicular dominance was associated with low or decreased follicular fluid concentrations of IGFBP-4 and -5
GH reduces mRNA and protein expression of IGFBP-5 in bovine mammary epithelial cells, but it does not affect the expression of IGFBP-3
The transgene in the cell clones was examined by polymerase chain reaction to verify that exogenous DNA (pKAP6-1 and IGFBP-5) had integrated stably into GFb cells
IGF-binding proteins prolong the half-life of the IGFs and have been shown to either inhibit or stimulate the growth promoting effects of the IGFs on cell culture. They alter the interaction of IGFs with their cell surface receptors.
, IGF-binding protein 5
, insulin-like growth factor-binding protein 5
, insulin-like growth factor binding protein-5
, insulin-like growth factor binding protein 5
, insulin-like growth factor binding protein 5a
, insulin-like growth factor binding protein 5b