KRR1 is a fundamental gene that encodes a small subunit processome component homolog, playing a crucial role in the biogenesis of the ribosomal 40S subunit. It is a protein coding gene, intricately involved in the early stages of pre-18S rRNA processing, a cornerstone process for the production of functional ribosomes. The KRR1 protein is involved in RNA binding activity and has been shown to be essential for cellular survival due to its involvement in ribosome assembly. The gene is expressed ubiquitously across various tissues, highlighting its importance in the fundamental operations of eukaryotic cells. Expression levels of KRR1 are indicative of a cell's ribosomal biogenesis activity, which is closely tied to the cell's growth and division cycles. Given its central role in the cellular machinery, the regulation of KRR1 expression is a finely tuned process, responsive to a variety of intracellular signals and extracellular cues.
Research has identified several chemical compounds that could serve as activators to induce the expression of KRR1. Compounds such as β-Estradiol are known to engage specific receptors that may lead to the transcriptional activation of genes involved in cell growth, which could include KRR1 due to its role in ribosome assembly. Similarly, DNA-binding agents like Mithramycin A might indirectly lead to an increase in KRR1 expression by altering transcriptional initiation processes. Agents that cause cellular stress, such as Tunicamycin, which inhibits N-linked glycosylation, can trigger a cellular response aiming to bolster ribosome production, stimulating an upregulation of KRR1 as a compensatory mechanism. Furthermore, the cellular response to DNA damage, as seen with compounds like Etoposide and Doxorubicin, may also prompt an elevation in KRR1 expression, as the need for ribosomal biogenesis can be heightened during the repair processes. It is important to note that while these compounds have been associated with changes in gene expression patterns, the direct relationship between these compounds and the specific induction of the KRR1 gene is a subject for rigorous scientific investigation. The complex interplay between these chemical compounds and the cellular environment underscores the delicate balance of gene expression regulation within the cell.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
β-Estradiol | 50-28-2 | sc-204431 sc-204431A | 500 mg 5 g | $62.00 $178.00 | 8 | |
β-Estradiol may upregulate KRR1 expression by engaging estrogen receptors, which can initiate transcriptional changes supporting cellular proliferation and rRNA processing requirements. | ||||||
Mithramycin A | 18378-89-7 | sc-200909 | 1 mg | $54.00 | 6 | |
Mithramycin A could trigger the upsurge in KRR1 expression by binding to GC-rich sequences in gene promoters, altering transcriptional initiation and ribosomal biogenesis pathways. | ||||||
Taxol | 33069-62-4 | sc-201439D sc-201439 sc-201439A sc-201439E sc-201439B sc-201439C | 1 mg 5 mg 25 mg 100 mg 250 mg 1 g | $40.00 $73.00 $217.00 $242.00 $724.00 $1196.00 | 39 | |
Through stabilization of microtubules, Taxol may indirectly stimulate KRR1 expression by activating signaling cascades that prompt cellular growth and corresponding increases in ribosomal assembly. | ||||||
Camptothecin | 7689-03-4 | sc-200871 sc-200871A sc-200871B | 50 mg 250 mg 100 mg | $57.00 $182.00 $92.00 | 21 | |
Camptothecin might induce KRR1 expression by eliciting DNA damage responses, necessitating augmented ribosomal biogenesis for repair processes. | ||||||
Methotrexate | 59-05-2 | sc-3507 sc-3507A | 100 mg 500 mg | $92.00 $209.00 | 33 | |
In response to Methotrexate's interference with nucleotide synthesis, cells may increase KRR1 expression to boost ribosome production and overcome deficits in nucleotide availability. | ||||||
Doxorubicin | 23214-92-8 | sc-280681 sc-280681A | 1 mg 5 mg | $173.00 $418.00 | 43 | |
Doxorubicin may provoke an elevation in KRR1 expression as part of a broader cellular response to DNA intercalation and the consequent demand for protein synthesis in repair mechanisms. | ||||||
Etoposide (VP-16) | 33419-42-0 | sc-3512B sc-3512 sc-3512A | 10 mg 100 mg 500 mg | $32.00 $170.00 $385.00 | 63 | |
Etoposide, by causing DNA strand breaks, could engender a surge in KRR1 expression to meet the heightened requirements for ribosome biogenesis during DNA damage repair. | ||||||
Cisplatin | 15663-27-1 | sc-200896 sc-200896A | 100 mg 500 mg | $76.00 $216.00 | 101 | |
The formation of DNA adducts by Cisplatin may lead to an upsurge in KRR1 expression as a cellular strategy to enhance ribosomal function for stress response protein synthesis. | ||||||
Tunicamycin | 11089-65-9 | sc-3506A sc-3506 | 5 mg 10 mg | $169.00 $299.00 | 66 | |
Tunicamycin's inhibition of glycosylation could precipitate an increase in KRR1 expression as part of the unfolded protein response, aiming to maintain ribosomal output under endoplasmic reticulum stress. | ||||||
Bortezomib | 179324-69-7 | sc-217785 sc-217785A | 2.5 mg 25 mg | $132.00 $1064.00 | 115 | |
Bortezomib may promote KRR1 expression through the accumulation of misfolded proteins, leading to a need for increased ribosomal production to manage proteotoxic stress. | ||||||