MTBP Antibody
- Known as:
- MTBP Antibody
- Catalog number:
- 2447
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- MTBP Antibody
Related genes to: MTBP Antibody
- Gene:
- MTBP NIH gene
- Name:
- MDM2 binding protein
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 8q24.12
- Locus Type:
- gene with protein product
- Date approved:
- 2000-08-23
- Date modifiied:
- 2016-10-05
Related products to: MTBP Antibody
Related articles to: MTBP Antibody
- Although MTBP is essential for replication origin firing, we show here that strong depletion of MTBP can have minor effects on DNA replication rates. This suggests an adaptive process in the DNA replication program, so we examined mechanisms underlying this plasticity. Using an auxin-inducible degron to deplete MTBP, we found that acute suppression of MTBP blocked DNA replication, but that replication rates recovered over time. The timing of this recovery paralleled S phase expression of Cyclin B1, and inhibition of CDK1-Cyclin B1 prevented the recovery. Recovery did not involve restoration of origin firing; instead, replication recovered through accelerated fork progression. Consistent with CDK1 driving this acceleration, ATR inhibition, which activates CDK1, stimulated DNA replication in MTBP-depleted cells through CDK1-dependent increased fork progression rather than increased origin firing. Knockdown of RIF1, a known CDK1 target, phenocopied this effect. Although RIF1 is best known for opposing DDK-dependent MCM phosphorylation at origins, we find that RIF1 knockdown stimulates replication even when DDK is inhibited. Furthermore, RIF1 loss increased replication by accelerating fork progression rather than increasing origin firing. Together, these findings reveal a CDK1-RIF1-dependent mechanism that promotes fork speed during S phase and defines a form of replication plasticity in which fork rate compensates for reduced origin firing. - Source: PubMed
Publication date: 2026/05/22
Hossain Md ShahadatSansam Courtney GDhar KrishanuSansam Christopher L - Eukaryotic cells license far more potential replication origins than they use, but how origin firing rate is tuned in S phase, especially under replication stress, remains unclear. Here, we identify a regulatory mechanism by which cyclin-dependent kinase (CDK) activity controls the abundance and chromatin recruitment of the origin firing factors TRESLIN and MTBP to promote dormant origin activation. Inhibition of WEE1 kinase during S phase increases CDK activity, which blocks the PCNA-CRL4-dependent degradation of TRESLIN and enhances its chromatin association along with MTBP. This increased loading is required for elevated helicase recruitment and DNA synthesis under CDK-hyperactive conditions. We define a sequence within TRESLIN required for its degradation and show that TRESLIN stabilization is necessary but not sufficient for CDK-driven origin firing. Replication stress regulates TRESLIN destruction in a dose- and time-dependent manner. Acute high-dose hydroxyurea suppresses CDK activity and reduces chromatin-bound TRESLIN, whereas prolonged low-dose hydroxyurea is accompanied by elevated CDK activity and increased chromatin loading of TRESLIN-MTBP and CDC45. Altogether, these findings uncover a control point in replication origin usage with implications for genome stability and therapeutic kinase inhibition. - Source: PubMed
Publication date: 2026/05/20
Hossain Md ShahadatSansam Courtney GWittig Kimberlie ANoble Tyler DBoyd Kevin ASansam Christopher L - Despite the near-complete elimination of cholera in many developing countries, numerous lower-income countries continue to face recurring epidemics. Although extensive research has been conducted on cholera transmission dynamics and control, a comprehensive approach to managing outbreaks in resource-limited settings remains elusive. This study introduces a cholera epidemic model incorporating a resource allocation strategy to balance efforts between reducing transmission and enhancing recovery rates. The model is validated using weekly cholera data from the resurgence in Haiti (October 2022-March 2023) to estimate key parameters and the control reproduction number . Based on these estimated parameters, the proposed model exhibits rich dynamical behavior, including backward and Hopf bifurcations, highlighting its potential for a multi-wave epidemic pattern. Using a continuous-time Markov chain (CTMC) model and the Gillespie algorithm, we calculate the extinction probability of cholera, comparing it with multitype branching process (MTbp) results, which estimate the analytical form of the probability of cholera extinction and outbreak, showing excellent agreement. Finally, construct a nonlinear programming problem (NLPP) to find the optimal combination of resources to minimize outbreak probability. In solving this NLPP, we find that prioritizing resources to recovery improve interventions is more effective than reducing transmission to minimize the probability of disease outbreak. These insights can guide resource allocation strategies to reduce cholera outbreaks in resource-constrained settings. - Source: PubMed
Publication date: 2026/05/13
Panda SudiptaHalder SujitChattopadhyay Joydev - Earlier detection of colorectal cancer (CRC) can improve survival rates. A simple, effective blood test may help improve screening participation. The multi-target blood protein (MTBP; ColoSTAT) test and algorithm uses concentrations of five protein biomarkers of CRC and patient's sex and age to generate a CRC likelihood score. We compared the performance of the MTBP test in detecting CRC to colonoscopy, the 'gold standard'. - Source: PubMed
Publication date: 2026/01/16
He Emily Yvan Hazel Guy ASloss Andrew MPianko StephenBrown Gregor JClingan Philip RSingh RajvinderSolterbeck Ann CTraficante RobertFormby-Miller LouiseLockett TrevorMacrae Finlay - Replication origins in human cells form clusters ranging from tens to hundreds of kilobases called initiation zones (IZs), typically located in intergenic regions between active genes. On a larger megabase scale, chromosomes replicate following temporally defined replication timing (RT), where euchromatic regions replicate early, and heterochromatic regions replicate late. Although the stochastic model of IZ firing with a temporally regulated limiting factor can explain RT formation, this limiting factor in human cells remains unclear. To investigate the relationship between IZ and RT, we map the temporal firing pattern of IZs and examine the genome-wide distributions of replication licensing and firing factors in human cells. We identify TRESLIN-MTBP as a key limiting firing factor for replication initiation. Its loading onto phosphorylated MCM2-7 double hexamer (MCM-DH) is controlled by the opposing phosphorylation events on MCM-DH by Dbf4-dependent kinase and RIF1-Protein Phosphatase 1, which ultimately determine IZs and establish RT. - Source: PubMed
Publication date: 2025/12/02
Zhu XiaoxuanBektash AtabekHatoyama YukiMuramatsu SachikoIsobe Shin-YaObuse ChikashiToyoda AtsushiDaigaku YasukazuChen Chun-LongKanemaki Masato T