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The protein encoded by SEC23B is a member of the SEC23 subfamily of the SEC23/SEC24 family, which is involved in vesicle trafficking. Zusätzlich bieten wir Ihnen Sec23 Homolog B (S. Cerevisiae) Antikörper (39) und Sec23 Homolog B (S. Cerevisiae) Kits (4) und viele weitere Produktgruppen zu diesem Protein an.
Showing 4 out of 6 products:
novel compound mutations of c.1727T>C and c.1831C>T of the SEC23B gene probably underlie the congenital dyserythropoietic anemia type II in the family
Mutation in SEC23B gene is associated with congenital dyserythropoietic anemia.
miR (zeige MLXIP Proteine)-130a is an epigenetically regulated miRNA involved in regulation of key molecular and phenotypic features of prostate carcinogenesis, acting as a tumour suppressor miRNA by targeting SEC23B and DEPDC1 (zeige DEPDC1 Proteine).
SEC23B-Y462C congenital dyserythropoietic anemia type II is only seen in a distinct Indian community (Vaish) in whom a recessively inherited shared haplotype can be showed, consistent with a founder effect.
Germline Heterozygous Variants in SEC23B Are Associated with Cowden Syndrome and Enriched in Apparently Sporadic Thyroid Cancer.
Congenital dyserythropoietic anemia, type II with SEC23B exon 12 c.1385 A --> G mutation, and pseudo-Gaucher cells in two siblings has been described.
ALG-2 (zeige PDCD6 Proteine) attenuates COPII budding in vitro and stabilizes the Sec23/Sec31A (zeige SEC31A Proteine) complex.
Both probands with congenital dyserythropoietic anemia IotaI in the second family were homozygotes of the SEC23B gene with mutation c.938G>A (R313H).
Mutations in SEC23B lead to congenital dyserythropoietic anemia type II due to alterations in coat protein (COP)II complex trafficking machinery. [REVIEW]
study identified four novel SEC23B mutations associated with ongenital dyserythropoietic anemia type II disease; also demonstrated that the genetic alteration results in a significant decrease of SEC23B transcript in erythroid precursors
SEC23B but not SEC23A (zeige SEC23A Proteine) is essential for murine pancreatic development.
Acinar Sec23b deletion results in induction of ER stress and increased apoptosis in the pancreas, potentially explaining the loss of pancreatic cells and decreased pancreatic weight. These findings demonstrate that SEC23B is required for normal function of pancreatic acinar cells in adult mice.
Results show that transplantation of SEC23B-deficient hematopoietic stem cells does not result in a hematopoietic stem cells phenotype.
In SEC23B-deficient embryonic pancreas, defects occur in exocrine and endocrine tissues shortly after differentiation.
The protein encoded by this gene is a member of the SEC23 subfamily of the SEC23/SEC24 family, which is involved in vesicle trafficking. The encoded protein has similarity to yeast Sec23p component of COPII. COPII is the coat protein complex responsible for vesicle budding from the ER. The function of this gene product has been implicated in cargo selection and concentration. Multiple alternatively spliced transcript variants have been identified in this gene.
SEC23-like protein B
, SEC23-related protein B
, protein transport protein Sec23B
, transport protein SEC23B
, SEC23-related protein A
, protein transport protein Sec23A