CDKN1B Antibody
- Known as:
- CDKN1B Antibody
- Catalog number:
- 32066
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- CDKN1B Antibody
Related genes to: CDKN1B Antibody
- Gene:
- CDKN1B NIH gene
- Name:
- cyclin dependent kinase inhibitor 1B
- Previous symbol:
- -
- Synonyms:
- KIP1, P27KIP1
- Chromosome:
- 12p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-09-14
- Date modifiied:
- 2016-10-05
Related products to: CDKN1B Antibody
Related articles to: CDKN1B Antibody
- A combination of endogenous hypercortisolism and primary hyperparathyroidism (PHPT) occurs rarely, few clinical cases are described in the literature. The causes of the development of such combination are poorly investigated. - Source: PubMed
Publication date: 2026/09/08
Mamedova E OPrzhiyalkovskaya E GRozhinskaya L YaYanar E AChugunov I SKolodkina A AVasilyev E VTiulpakov A NBelaya Zh EMelnichenko G A - Low-variant allele frequency (VAF) variants identified during germline testing may represent constitutional mosaicism or acquired somatic events restricted to hematopoietic cells. Although clonal hematopoiesis of indeterminate potential (CHIP) has emerged as an important source of interpretative pitfalls in hereditary cancer testing, its potential impact on the interpretation of CDKN1B variants has not been specifically emphasized. We aimed to determine whether low-VAF CDKN1B variants detected during routine germline testing for pituitary adenoma predisposition may represent clonal hematopoiesis rather than true constitutional alterations. We analyzed patients referred for routine genetic investigation of pituitary adenoma predisposition who has low-frequency CDKN1B variants identified in blood-derived DNA. Additional analyses were performed, including assessment of variant distribution in nonhematopoietic tissues, tumor DNA analysis, and investigation of CHIP-associated genes. Three unrelated patients carrying truncating CDKN1B variants were identified, with blood-derived VAFs ranging from 4% to 6%. Clinical presentations included 2 gonadotroph macroadenomas diagnosed later than age 70 years and 1 prolactin-secreting macroadenoma diagnosed before age 35. CDKN1B variants were absent in buccal swab DNA and from available pituitary tumor DNA. Additional pathogenic variants affecting CHIP-associated genes were identified in 2 individuals. Collectively, these findings supported a leukocyte-restricted origin of the CDKN1B variants and suggested CHIP as the most likely explanation. Low-frequency CDKN1B variants detected during blood-based germline testing should not automatically be interpreted as constitutional mosaicism or inherited endocrine tumor predisposition. Integration of tissue-specific analyses and consideration of CHIP-related findings are essential to avoid inappropriate genetic counseling, unnecessary familial investigations, and misleading surveillance recommendations. - Source: PubMed
Chansavang AlbainFriedrich ChloéKuhn EmmanuelleToussaint AurélieGodin AlimhaHamzaoui NadimBertherat JérômeKosmider OlivierPasmant Eric - Colorectal cancer (CRC) is one of the most prevalent causes of cancer-associated deaths globally, largely driven by non-responsiveness to drugs and metastatic progression. Natural product-derived multi-targeted anticancer agents have emerged as a promising strategy to treat or relieve various cancer conditions, including CRC. To investigate the therapeutic potential of natural bioactive compounds against colorectal cancer, we examined the effects of Juglone (5-hydroxy-1,4-naphthoquinone, [Formula: see text]), a naturally occurring constituent of the Juglandaceae family, on the human colorectal cancer cell lines HCT116 and HT-29. Flow cytometric analysis demonstrated that Juglone markedly increased early and late apoptotic cell populations, with minimal necrosis. This apoptotic effect was further confirmed by enhanced activation of caspase-3/7, -8, and - 9, indicating the involvement of both intrinsic and extrinsic apoptotic pathways. At the transcriptional level, Juglone upregulated pro-apoptotic genes (BAX, CASP3, CASP8, CASP9) while downregulating the anti-apoptotic gene BCL2, supporting a shift toward programmed cell death. Cell cycle analysis revealed significant G0/G1 phase arrest in both CRC cell lines, accompanied by suppression of CCND1, CCNB1, CDK2, and CDK4 and upregulation of CDKN1A (p21) and CDKN1B (p27). Juglone modulated key oncogenic signaling pathways by downregulating ERK1/2 and AKT1 while upregulating p38 and JNK1. Functionally, Juglone significantly suppressed cancer cell migration and invasion, indicating anti-metastatic potential. Collectively, these findings demonstrate that Juglone exerts potent anticancer effects by targeting multiple processes involved in colorectal cancer progression, including proliferation, apoptosis, cell cycle regulation, survival signaling, and metastasis. These findings demonstrated that Juglone markedly inhibited cell viability in a concentration- and time-dependent manner, exhibiting potent cytotoxic activity with IC₅₀ values in the low micromolar range after 48 h of treatment. Therefore, Juglone may represent a promising multi-targeted therapeutic candidate for colorectal cancer, warranting further in vivo evaluation. - Source: PubMed
Publication date: 2026/08/25
Deebani Afnan OAnwar Kanzy M AAnwar Yousra M AAlsahafi SameerhKaabi Aaishah M HAlotaibi Mashael AMohammedsaleh Zuhair MSembawa Hatem ASoliman Mona HAlmohaimeed Hailah M - Genetic testing of patients with pituitary adenomas enables delivery of genotype-based precision care. Germline testing might identify variants predisposing to formation of pituitary adenomas and, potentially, other neoplasms. These include loss-of-function variants in AIP, MEN1, CDKN1B, PRKAR1A, SDHA, SDHB, SDHC, SDHD and MAX; GPR101-containing Xq26.3 microduplications; and postzygotic gain-of-function GNAS variants. Somatic testing might help identify and manage aggressive pituitary adenoma types and very rarely encountered pituitary carcinomas. This Pituitary Society Consensus Statement provides evidence-based guidance on the clinical application of these genetic tests, focusing on germline genetic testing, with recommendations regarding genes for inclusion in panel testing, test indications, pre-test counselling, test methodologies, and the interpretation and follow-up of results. As somatic genetic testing is gradually becoming available in clinical practice, recommendations are provided regarding clinical scenarios in which somatic testing might be considered and which genes to test. The consensus group concluded that genetic testing is an increasingly valuable adjunct in the assessment and management of people with pituitary adenomas. When indicated, genetic testing should ideally be undertaken within a multidisciplinary team comprising endocrine, genetic and laboratory expertise to ensure high-quality testing and safe and effective result interpretation and follow-up. - Source: PubMed
Publication date: 2026/08/25
De Sousa Sunita M CAndoniadou Cynthia LDaly Adrian FGadelha MônicaGatto FedericoKamenický PeterMarques PedroReincke MartinRuf-Zamojski FrederiqueSalvatori RobertoTakahashi YutakaTatsi ChristinaAraki TakakoChiloiro SabrinaDichtel LauraIoachimescu Adriana GMallea-Gil SusanaNiculescu Dan APereira Alberto MShimon IlanWass JohnZada GabrielFleseriu MariaMelmed Shlomo - Sunitinib is associated with a higher incidence of thrombocytopenia than other molecularly targeted drugs. However, the underlying mechanism remains unclear. Because platelets are derived from megakaryocytes originating from hematopoietic progenitor cells in the bone marrow, sunitinib is presumed to interfere with megakaryocyte proliferation, maturation, or platelet production. Therefore, megakaryocytes play a crucial role in elucidating the mechanism of sunitinib-induced thrombocytopenia. However, in vivo sampling of megakaryocytes is challenging due to the invasiveness of bone marrow collection and the limited cell yield. Accordingly, we investigated the mechanism of thrombocytopenia induced by sunitinib and its active metabolite, N-desethyl sunitinib, using human induced pluripotent stem cell-derived immortalized megakaryocyte cell lines (imMKCLs). Both sunitinib and N-desethyl sunitinib suppressed the proliferation and cell division of imMKCLs. Furthermore, RNA sequencing revealed downregulation of cell cycle-related genes. Although the expression of cyclin-dependent kinase inhibitors, CDKN1A and CDKN1B, was significantly increased, polyploidization in imMKCLs remained unaffected. In conclusion, sunitinib and N-desethyl sunitinib induce thrombocytopenia by inhibiting the proliferation of immature megakaryocytes through suppression of cell cycle progression. - Source: PubMed
Publication date: 2026/07/14
Iwasaki MoemiHashita TadahiroHori EiseiNakamura SouEto KojiHashimoto YutakaMatsunaga TamihideIwao Takahiro