Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher tous les synonymes
Human Monoclonal SALL4 Primary Antibody pour IHC (p), ELISA - ABIN566099
Cauffman, De Rycke, Sermon, Liebaers, Van de Velde: Markers that define stemness in ESC are unable to identify the totipotent cells in human preimplantation embryos. dans Human reproduction (Oxford, England) 2008
Show all 17 Pubmed References
Human Polyclonal SALL4 Primary Antibody pour ELISA, WB - ABIN4369825
Paradisi, Arias: IVIC syndrome is caused by a c.2607delA mutation in the SALL4 locus. dans American journal of medical genetics. Part A 2007
Show all 3 Pubmed References
Rat (Rattus) Polyclonal SALL4 Primary Antibody pour ELISA, WB - ABIN253101
Wang, Rao, Chu, Shen, Levasseur, Theunissen, Orkin: A protein interaction network for pluripotency of embryonic stem cells. dans Nature 2006
Human Polyclonal SALL4 Primary Antibody pour WB - ABIN388303
Yang, Chai, Liu, Fink, Lin, Silberstein, Amin, Ward, Ma: Bmi-1 is a target gene for SALL4 in hematopoietic and leukemic cells. dans Proceedings of the National Academy of Sciences of the United States of America 2007
Show all 2 Pubmed References
Data show that both sall1 (Montrer SALL1 Anticorps) and sall4 act to repress pou5f3 (oct4)family gene expression in the neural plate, thereby allowing vertebrate neural development to proceed.
These results suggest that Sall4, activated by posteriorizing signals, represses the pou5f3 genes to provide a permissive environment.
SAL family member (XlSALL4) is expressed at the right place and time to play a role regulating both digit identity along the anterior/posterior axis and epimorphic limb regeneration
Sall4 expression expression in chemosensory cells implicates this transcription factor in the development and renewal of taste epithelia in zebrafish.
Sall gene family redundancy and tbx5 (Montrer TBX5 Anticorps) offer explanations for the similarity of individuals with Okihiro syndrome and Holt-Oram syndrome limb defects
Findings indicate that SALL4 critically contributes to MLL (Montrer MLL Anticorps)-AF9 (Montrer MLLT3 Anticorps)-induced leukemia, unraveling the underlying transcriptional and epigenetic mechanisms in this disease.
SALL4 associated with the NuRD co-repressor and repressed expression of the tumor suppressor genes Foxl1 (Montrer FOXL1 Anticorps) and Dusp4 (Montrer DUSP9 Anticorps).
Study propose a model whereby enhancer binding by Sall4 and other pluripotency-associated transcription factors is responsible for maintaining the balance between transcriptional programmes in pluripotent cells.
SALL4 has a negative impact in DNA damage repair, and support the model of dual functional properties of SALL4 in leukemogenesis through inhibiting DNA damage repair and promoting cell survival.
these data reveal the full profile of PLZF (Montrer ZBTB16 Anticorps) and SALL4 regulatory targets in undifferentiated spermatogonia.
study explores a pivotal role of Sall4 in regulating epigenetic maturation of mouse oocytes.
JARID2 (Montrer JARID2 Anticorps) physically interacts with ESRRB (Montrer ESRRB Anticorps), SALL4A, and PRDM14 (Montrer PRDM14 Anticorps)
As SALL4A is known to impair ZBTB16 (Montrer ZBTB16 Anticorps)-mediated Kit repression , our study provides novel insights into the molecular mechanism by which ATRA could control KIT expression, and thereby the differentiation of Aal into A1 spermatogonia in vivo.
In differentiated ESCs (Montrer NR2E3 Anticorps), Sall4 bound to these somatic cell program gene loci, which are reportedly occupied by Prdm1 (Montrer PRDM1 Anticorps) in embryonic carcinoma cells.
This study identified a critical role of the Sall4-Gli3 (Montrer GLI3 Anticorps) system at the early steps of limb development for proper development of the appendicular skeletal elements.
Study showed significantly high expression of SALL4 mRNA in glioma specimens as compared to non-tumor samples using RT-PCR. Blocking SALL4 using SALL4-siRNA decreased proliferation of U87 and U251 cells, which was reversed by the addition of PTEN inhibitor phen (bpv). Furthermore, marked increase in PTEN mRNA and protein levels was seen in cells treated with siRNA-SALL4.
SALL4 is a promising prognostic biomarker for cancer, and is appropriate for the assessment of cancer prognosis in the Chinese people.
Our experimental data indicated that over expression of SALL4 was found in CRC (Montrer CALR Anticorps) and low expression of SALL4 was connected with high survival rate after surgery. Thus our study suggested that SALL4 could serve as a potential diagnostic and prognostic marker of CRC (Montrer CALR Anticorps).
SALL4 is a target gene of miR (Montrer MLXIP Anticorps)-181b in glioma.SALL4 is upregulated in glioma.
SALL4 is a target gene of mir (Montrer MLXIP Anticorps)-98 in non-small cell lung cancer cells.
miR (Montrer MLXIP Anticorps)-98 plays a suppressive role in the proliferation, migration, invasion and EMT (Montrer ITK Anticorps) of HCC (Montrer FAM126A Anticorps) cells, partly at least, via directly inhibition of SALL4.
SALL4 immunopositivity is not a prognostic factor in Combined hepatocellular carcinoma (HCC (Montrer FAM126A Anticorps)) and cholangiocarcinoma (CC) (cHCC-CC); however, it is associated with alpha-fetoprotein (Montrer AFP Anticorps), glypican 3 (Montrer GPC3 Anticorps) and EpCAM (Montrer EPCAM Anticorps) immunopositivity, indicating the mechanism of carcinogenesis.
these data suggest that Bmi-1 (Montrer BMI1 Anticorps) could serve as a novel prognostic biomarker in pediatric primary acute lymphoblastic leukemia (ALL)and may be partially regulated by Sall4a. Our study also showed that Bmi-1 (Montrer BMI1 Anticorps) could serve as a new therapeutic target for the treatment of pediatric ALL.
SALL4 overexpression is associated with neoplasms.
Findings indicate that long-term exposure to IM results in dysregulation of stem cell renewal-regulatory Hippo (MST1 (Montrer MST1 Anticorps)/2)/YAP (Montrer YAP1 Anticorps) signaling, and that inhibition of miR (Montrer MLXIP Anticorps)-181a using a microRNA sponge inhibitor resulted in decreased transcription of SOX2 (Montrer SOX2 Anticorps) and SALL4.
The protein encoded by this gene may be a zinc finger transcription factor. Defects in this gene are a cause of Duane-radial ray syndrome (DRRS).
sal-like 4 (Drosophila)
, sal-like protein 4-like
, sal-like 4
, zinc finger transcription factor SALL4 a
, sal-like protein 4
, zinc finger protein SALL4
, zinc finger protein 797