TheSox-13Gene: Structure, Promoter Characterization, and Chromosomal Localization

Roose, Jeroen P.; Korver, Wouter; Boer, Rosalie de; Kuipers, Jeroen; Hurenkamp, Jolanda

doi:10.1006/geno.1999.5779

Cited by 18 publications

(12 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…3a,b). The stop codon was upstream of the DNA-binding HMG domain, but downstream of the leucine zipper and glutamine-rich region 22, 23 . We confirmed by Sanger sequencing that this mutation was present in B6.SJL/NCI and B6.SJL/Tac mice, but absent from B6.SJL/Jax and B6.SJL/CR mice.…”

Section: Resultsmentioning

confidence: 99%

Deficiency in IL-17-committed Vγ4+ γδ T cells in a spontaneous Sox13-mutant CD45.1+ congenic mouse substrain provides protection from dermatitis

et al. 2013

View full text Add to dashboard Cite

IL-17-committed γδ T (γδT17) cells participate in many immune responses but their developmental requirements and subset specific functions remain poorly understood. Here we report that a commonly used CD45.1+ congenic C57BL/6 mouse substrain is characterized by a selective deficiency in Vγ4+ γδT17 cells. This trait is due to a spontaneous mutation in the transcription factor Sox13 that causes an intrinsic defect in development of these cells in the neonatal thymus. γδT17 cells migrate at low rates from skin to lymph nodes. In a model of psoriasis-like dermatitis, Vγ4+ γδT17 cells expand markedly in lymph nodes and home to inflamed skin. Sox13 mutant mice are protected from psoriasis-like skin changes, identifying a role for Sox13-dependent γδT17 cells in this inflammatory condition.

show abstract

Section: Resultsmentioning

confidence: 99%

Deficiency in IL-17-committed Vγ4+ γδ T cells in a spontaneous Sox13-mutant CD45.1+ congenic mouse substrain provides protection from dermatitis

et al. 2013

View full text Add to dashboard Cite

show abstract

“…Alternatively, antibody raised against SOX5 or SOX6 might cross-react SOX13 because the HMG box has high homology among these SOX D group protein. 18 p53 is previously reported to be recognized by T cells from patients with pancreatic cancer, 19 and frequently recognized by serum IgG Ab in patients with various cancers including colon cancers. [20][21][22] However, the particular p53 clone isolated in our study was recognized by sera from patients with a limited cancer including pancreatic cancer and was not recognized by sera from colon cancer patients.…”

Section: Discussionmentioning

confidence: 97%

Immune responses to DNA mismatch repair enzymes hMSH2 and hPMS1 in patients with pancreatic cancer, dermatomyositis and polymyositis

Okada

Noji

Goto

et al. 2005

Intl Journal of Cancer

View full text Add to dashboard Cite

To identify tumor antigens useful for diagnosis and immunotherapy of patients with pancreatic ductal adenocarcinoma, we applied a SEREX approach with a cDNA library made from 5 pancreatic cancer cell lines and sera obtained from 8 patients with pancreatic cancer, and isolated total 32 genes, including 14 previously characterized genes and 18 genes with unknown functions. Among these isolated antigens, serum IgG antibodies for 2 isolated DNA mismatch repair enzymes, Homo sapiens mutS homolog 2 (hMSH2) and Homo sapiens postmeiotic segregation increased 1 (hPMS1), were detected in patients with pancreatic ductal adenocarcinoma and dermatomyositis (DM), and polymyositis (PM), but not in sera from healthy individuals. Immunohistochemical study demonstrated that hMSH2 and hPMS1 were over-expressed in pancreatic ductal adenocarcinoma compared to normal pancreatic ducts. These results suggested that hMSH2 and hPMS1 may be useful as CD41 helper T cell antigens for immunotherapy of pancreatic cancer patients and that serum IgG antibodies may be useful for diagnosis of patients with pancreatic ductal adenocarcinoma and DM/PM. ' 2005 Wiley-Liss, Inc.Key words: SEREX; tumor antigens; pancreatic cancer; DNA mismatch repair enzyme Early diagnosis and curative treatment are still difficult for pancreatic ductal adenocarcinoma despite of increased incidence rate.

show abstract

“…One of them is the SOX9 gene, located at 17q, that has been shown to be involved in rearrangements with other autosomes, abnormalities which, by themselves, have caused sex ambiguity [28,29]. In a recently reported case with genitourinary malformations, a balanced translocation [t(1;18)(q32.1;q22.1)] karyotype [12] involved a gene responsible for genitourinary development on 18q32.1 [30] and a SOX gene on the 1q32.1 region [31].…”

Section: Discussionmentioning

confidence: 99%

Two unbalanced translocations involving a common 6p25 region in two XY female patients

et al. 2001

View full text Add to dashboard Cite

We report two 46,XY female patients with two different de novo unbalanced translocations, each involving the chromosomal region 6p25. The patient with a 46,XY,der(6)t(X;6)(p21.2;p25) karyotype had a sex reversal phenotype. The patient with a 46,XY,der(13)t(6;13)(p25;q33) karyotype had a male pseudohermaphrodite phenotype. Multi-paint fluorescent in situ hybridization was performed to determine the origin of the derivative material on 6p and 13q. The association of abnormalities of the 6p25 region with either an Xp duplication or a 13q deletion is reported here for the first time.

show abstract

TheSox-13Gene: Structure, Promoter Characterization, and Chromosomal Localization

Cited by 18 publications

References 24 publications

Deficiency in IL-17-committed Vγ4+ γδ T cells in a spontaneous Sox13-mutant CD45.1+ congenic mouse substrain provides protection from dermatitis

Deficiency in IL-17-committed Vγ4+ γδ T cells in a spontaneous Sox13-mutant CD45.1+ congenic mouse substrain provides protection from dermatitis

Immune responses to DNA mismatch repair enzymes hMSH2 and hPMS1 in patients with pancreatic cancer, dermatomyositis and polymyositis

Two unbalanced translocations involving a common 6p25 region in two XY female patients

Contact Info

Product

Resources

About