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anti-Human SOX10 Antibodies:
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Human Monoclonal SOX10 Primary Antibody for IHC, ELISA - ABIN1724912
Bannykh, Stolt, Kim, Perry, Wegner: Oligodendroglial-specific transcriptional factor SOX10 is ubiquitously expressed in human gliomas. in Journal of neuro-oncology 2006
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Human Monoclonal SOX10 Primary Antibody for FACS, ELISA - ABIN1724911
Shin, Vincent, Cuda, Xu, Kang, Kim, Taube: Sox10 is expressed in primary melanocytic neoplasms of various histologies but not in fibrohistiocytic proliferations and histiocytoses. in Journal of the American Academy of Dermatology 2012
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Human Monoclonal SOX10 Primary Antibody for IHC (p), ELISA - ABIN520385
Kim, Chang, Yeo, Haw, Kim: Histopathological study of the treatment of melasma lesions using a low-fluence Q-switched 1064-nm neodymium:yttrium-aluminium-garnet laser. in Clinical and experimental dermatology 2013
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Human Polyclonal SOX10 Primary Antibody for IHC, IHC (p) - ABIN5663150
Ivanov, Panaccione, Nonaka, Prasad, Boyd, Brown, Guo, Sewell, Yarbrough: Diagnostic SOX10 gene signatures in salivary adenoid cystic and breast basal-like carcinomas. in British journal of cancer 2013
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Human Polyclonal SOX10 Primary Antibody for IHC (p), WB - ABIN652035
Li, Tsuneki, Krauthammer, Couture, Schwartz, Madri: Modulation of Sox10, HIF-1?, Survivin, and YAP by Minocycline in the Treatment of Neurodevelopmental Handicaps following Hypoxic Insult. in The American journal of pathology 2015
Cow (Bovine) Polyclonal SOX10 Primary Antibody for IHC, WB - ABIN2777864
Wilson, Olm-Shipman, Acevedo, Palaniyandi, Hall, Kosa, Stumpff, Smith, Pitstick, Liao, Bjork, Czirok, Saadi: SPECC1L deficiency results in increased adherens junction stability and reduced cranial neural crest cell delamination. in Scientific reports 2016
A heterozygous nonsense mutation [substitution; position 127; cytosine to thymine (c.127C>T)] was identified in exon 2 of SOX10 (transcript ID: NM_006941.3) in the proband and the mother; however, not in other family members or healthy controls
This study showed that there is no evidence for the role of SOX10 in ependymocytes.
SOX10 can regulate the proliferation and tumor formation of gastric cancer by regulating the expression of CMTM7.
Characterization of novel SOX10 mutations in patients with Kallmann syndrome that showed reduced capacity to transactivate.
SOX10 was positively correlated with WT1, but negative correlated with androgen receptor+ subtypes
Enhanced SOX10 and KIT expression in cutaneous melanoma.
SOX10 might promote prostate cancer progression by accelerating the ability of the proliferation and invasion of prostate cancer cells
Expression of HMB45, MelanA and SOX10 is evident but exceedingly rare in non-small cell lung cancer cases
SOX10 was up-regulated in melanoma and negatively correlated with miR-31.
there have been a number of related reports that mutation of SOX10 will lead to Kallmann syndrome with deafness.
phylogenetic analysis and three-dimensional modelling of the SOX10 protein confirmed that the c.1333delT heterozygous mutation was pathogenic, indicating that this mutation might constitute a candidate disease-causing mutation.
Use of reliable positive and negative tissue controls is an important issue that must be addressed in any immunohistochemical staining reaction.4 SOX10 is a challenging marker in this sense, as no easy accessible tissues with consistent low-level expression have been identified at this time
High SOX10 expression is associated with Basal Breast Cancers.
Data show that depletion of SRY (sex determining region Y)-box 10 protein (SOX10) sensitizes mutant proto-oncogene proteins B-raf (BRAF) melanoma cells to RAF inhibitors in vitro and in vivo.
SOX10 immunohistochemistry may be of utility in distinguishing some of the varying adnexal tumors from each other, and from basal cell carcinoma (BCC), but given the staining of both apocrine and eccrine tumors, does not seem to provide information as to their origins as either eccrine or apocrine tumors.
Adenocarcinomas or adenomas derived from pigmented ciliary epithelium is distinguished from uveal melanoma by the absence of SOX10 expression and presence of the BRAF V600E mutation.
Therefore, the mutant cannot transactivate the MITF promoter effectively, inhibiting melanin synthesis and leading to WS2. Our study confirmed haploinsufficiency as the underlying pathogenesis for WS2.
Sox10 labeling is seen in a subset of metastatic triple-negative breast carcinomas, supporting its use as a marker of breast origin in this setting.
SOX10 is useful in the differential diagnosis of salivary gland neoplasms.
An extended immunohistochemical panel that includes beta-catenin and SOX10 helps to support the diagnosis of biphenotypic sinonasal sarcoma without the need for gene rearrangement studies.
The activity of Sox-10 transcription factor is well conserved and is regulated by SUMOylation.
In this study, we generated a mouse model, in which the SOX10 Q377X mutation was introduced into the Sox10 locus in such a way that Sox10 Q377X is constitutively expressed. Heterozygous mice carrying this mutation exhibited pigmentation and enteric nervous system defects. We found no phenotypic evidence for neurological defects in peripheral or central nervous systems.
SOX10 was significantly increased in nasopharyngeal carcinoma tissues and cell lines
Study shows the conversion of mouse skin fibroblasts into induced Schwann cells by driving the expression of two transcription factors, Sox10 and Egr2.
Both Sox10 and Sox8 were found to be jointly required for myelin maintenance and myelin gene expression.
This study demonstrated that Transcription factor Sox10 regulates oligodendroglial Sox9 levels via microRNAs.
data further our understanding of SOX10 protein regulation and provide critical information for identification of molecular pathways that modulate SOX10 protein levels in melanoma, with the ultimate goal of discovering novel targets for more effective combinatorial therapeutic approaches for melanoma patients
BRG1 is a SOX10 co-activator, required to establish the melanocyte lineage and promote expression of genes important for melanocyte function.
This study demonstrates that Sox10(+) cells contribute to pericytes and smooth muscle cells in most parts of the body, including those from neural crest and non-neural crest, which has significant implications in vascular remodeling under physiological and pathological conditions.
Chd7 coordinates with Sox10 to regulate the initiation of myelinogenesis and acts as a molecular nexus of regulatory networks that account for the development of a seemingly diverse array of lineages, including oligodendrocytes and osteoblasts, pointing to previously uncharacterized Chd7 functions.
We discovered that Tead1 and co-activators Yap and Taz are required for Pmp22 expression, as well as for the expression of Egr2 Tead1 directly binds Pmp22 and Egr2 enhancers early in development and Tead1 binding is induced during myelination, correlating with Pmp22 expression. The data identify Tead1 as a novel regulator of Pmp22 expression during development in concert with Sox10 and Egr2
SOX10 directly activates MCM5 transcription by binding to conserved SOX10 consensus DNA sequences in the MCM5 promoter.
Control of differentiation of mouse enteric nervous system progenitor cells by EDN3 requires regulation of Ednrb expression by SOX10 and ZEB2.
Kaiso and Sox10 sequentially interact with Tcf7l2 to coordinate the maturation of oligodendrocyte.
Findings uncover a central role of SOX10 as a global regulator of gene expression in the melanocyte lineage by targeting diverse regulatory pathways.
Ets1 and Sox10 interact to promote proper melanocyte and enteric ganglia development from the neural crest.
Sox10(rtTA/+) driven reporter expression in the cochlea persists for at least 54 days after cessation of neonatal induction
Disrupted SOX10 function causes spongiform neurodegeneration in gray tremor mice.
Our findings provide proof-of-concept that Sox10 can convert conducive cells into oligodendrocyte-like cells in vivo and delineates options for future therapeutic strategies.
Conditional deletion of the neural crest specific transcription factor, Sox10, using the rhombic lip/neural crest specific Wnt1-cre driver spares Sox10 expression in the ear.
This is strongly reminiscent of the situation in Schwann cells where Sox10 first induces and then cooperates with Krox20 during myelination
findings reveal surprising diversity in even the mode of the interactions between Sox5 and Sox10 governing specification of pigment cell types in medaka and zebrafish, and suggest that this is related to the evolution of a fourth pigment cell type
This study reveals a unique regulatory mechanism, the Rgs2-Ppard-Sox10 signaling cascade, and defines a key molecular regulator, Rgs2, in neural crest development.
Our zebrafish CHARGE model thus reveals important regulatory roles for Chd7 at multiple points of neural crest development viz., migration, fate choice and differentiation and we suggest that sox10 deregulation is an important driver of the neural crest-derived aspects of Chd7 dependent CHARGE syndrome.
Demonstrate a contribution of sox10-dependent cranial neural crest to olfactory sensory neurons in zebrafish and provide important insights into the assembly of the nascent olfactory system.
Data indicate that the optical flow analysis detected and quantified significant differences in the cell migrations of Sox10:EGFP positive cranial neural crest cells in ethanol treated versus untreated embryos.
Sox10 might not be required for neural crest formation but is important for later steps during neural crest development.
prdm1a Regulates sox10 and islet1 in the development of neural crest and Rohon-Beard sensory neurons.
Sox10 function is necessary for the survival of myelinating oligodedrocytes subsequent to axon wrapping but is not required for the survival of nonmyelinating oligodendrocyte progenitor cells.
Phox2b function is sox10-dependent in the developing enteric nervous system
Decrement of function of foxd3 and/or sox10, two genes important for the development and specification of neural crest, resulted in a reduction and/or loss of GnRH cells of the midbrain, as well as a reduction in the number of terminal nerve GnRH cells.
Data show that expression of Mitf rescues pigmentation fully in zebrafish, but only partially in Sox10-mutant mice.
Sox10 is expressed transiently in the sensory neuron lineage, and specifies sensory neuron precursors by regulating the proneural gene neurogenin1.
Sox10 has diverse roles in the otic vesicle that may be important in a zebrafish model for Waardenburg syndrome type IV
Disc1 functions in the transcriptional repression of foxd3 and sox10, thus mediating cranial neural crest cell migration and differentiation.
This gene encodes a member of the SOX (SRY-related HMG-box) family of transcription factors involved in the regulation of embryonic development and in the determination of the cell fate. The encoded protein may act as a transcriptional activator after forming a protein complex with other proteins. This protein acts as a nucleocytoplasmic shuttle protein and is important for neural crest and peripheral nervous system development. Mutations in this gene are associated with Waardenburg-Shah and Waardenburg-Hirschsprung disease.
SRY-related HMG-box gene 10
, dominant megacolon, mouse, human homolog of
, transcription factor SOX-10
, SRY-box containing gene 10
, Sry-boxntranscription factor, SOX-10
, transcription factor Sox-10
, transcription factor Sox10
, SRY-box 10
, SRY (sex determining region Y)-box 10
, transcription factor SOX-10-like
, transcription factor sox10
, dominant megacolon
, transcription factor SOX-M
, SRY (sex determining region Y)-box 9 (campomelic dysplasia, autosomal sex-reversal)